Atlas of Pain Management Injection Techniques E-Book
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949 pages
English

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Description

Master every essential pain management injection technique used today with Atlas of Pain Management Injection Techniques, 3rd Edition. With expert tips from leading authority Steven D. Waldman, MD, JD and abundant step-by-step color illustrations, you’ll see how to evaluate the causes of pain, identify the most promising injection approach, locate the injection site with precision, and deliver the relief your patients crave. From the head and neck to the foot and ankle - and everywhere between - this best-selling pain management reference equips you to perform a complete range of clinical injection techniques with greater confidence!

  • Consult this title on your favorite e-reader with intuitive search tools and adjustable font sizes. Elsevier eBooks provide instant portable access to your entire library, no matter what device you're using or where you're located.
  • Perform each technique like an expert and avoid complications with clinical pearls in each chapter.
  • Diagnose pain syndromes effectively with updated coverage encompassing the latest identification guidelines and definitions.
  • See exactly how to proceed and fully understand the nuances of each technique thanks to hundreds of illustrations - many in full color, many new to this edition - demonstrating relevant anatomy, insertion sites, and more.

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Informations

Publié par
Date de parution 30 août 2012
Nombre de lectures 0
EAN13 9781455728145
Langue English
Poids de l'ouvrage 9 Mo

Informations légales : prix de location à la page 0,0731€. Cette information est donnée uniquement à titre indicatif conformément à la législation en vigueur.

Exrait

Atlas of Pain Management Injection Techniques
Third Edition

Steven D. Waldman, MD, JD
Clinical Professor of Anesthesiology, Professor of Medical Humanities and Bioethics, University of Missouri–Kansas City School of Medicine, Kansas City, Missouri

Saunders
Table of Contents
Cover image
Title page
Copyright
Dedication
Preface
Acknowledgments
Section 1: Head and Neck
Chapter 1: Temporomandibular Joint Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 2: Supraorbital Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 3: Trochlear Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 4: Buccal Fold Injection for Incisors and Canine Teeth
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 5: Buccal Fold Injection Technique for Upper Premolar Teeth
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 6: Buccal Fold Injection for Upper Molar Teeth
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 7: Incisive Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 8: Inferior Alveolar Nerve Block for Lower Premolar Teeth
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 9: Inferior Alveolar Nerve Block for Lower Molar Teeth
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 10: Styloid Process Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 11: Stylohyoid Ligament Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 12: Nasociliary Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 13: Auriculotemporal Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 14: Omohyoid Muscle Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 15: Trigeminal Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 16: Injection Technique for Trapezius Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 17: Injection Technique for Cervical Strain
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 18: Injection Technique for Sternocleidomastoid Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 19: Occipital Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 20: Injection Technique for Splenius Cervicis Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Section 2: Shoulder
Chapter 21: Intraarticular Injection of the Shoulder Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 22: Acromioclavicular Joint Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 23: Supraspinatus Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 24: Infraspinatus Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 25: Subscapularis Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 26: Injection Technique for Deltoid Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 27: Injection Technique for Pectoralis Major Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 28: Injection Technique for Pectoralis Major Tear Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Differential Diagnosis
Side Effects and Complications
Chapter 29: Injection Technique for Teres Major Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 30: Bicipital Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 31: Injection Technique for Subacromial Impingement Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 32: Injection Technique for Os Acromiale Pain Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 33: Injection Technique for Biceps Brachii Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 34: Injection Technique for Triceps Brachii Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 35: Injection Technique for Rotator Cuff Tear
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 36: Injection Technique for Quadrilateral Space Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 37: Subdeltoid Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 38: Subcoracoid Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 39: Injection Technique for Frozen Shoulder Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 40: Injection Technique for Scapulocostal Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Section 3: Elbow and Forearm
Chapter 41: Intraarticular Injection of the Elbow Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 42: Injection Technique for Anconeus Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 43: Injection Technique for Anconeus Epitrochlearis
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 44: Ulnar Nerve Block at the Elbow
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 45: Injection Technique for Driver’s Elbow
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 46: Injection Technique for Os Supertrochleare Related Elbow Pain
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 47: Lateral Epicondyle Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 48: Radial Nerve Block at the Humerus
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 49: Medial Epicondyle Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 50: Triceps Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 51: Olecranon Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 52: Cubital Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 53: Injection Technique for Supinator Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 54: Injection Technique for Extensor Carpi Ulnaris Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 55: Injection Technique for Extensor Carpi Radialis Longus Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 56: Injection Technique for Flexor Carpi Ulnaris Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 57: Injection Technique for Flexor Carpi Radialis Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 58: Median Nerve Block at the Elbow
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 59: Median Nerve Block below Elbow
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 60: Lateral Antebrachial Cutaneous Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Section 4: Wrist and Hand
Chapter 61: Intraarticular Injection of the Wrist Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 62: Intraarticular Injection of the Radioulnar Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 63: Flexor Carpi Radialis Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 64: Flexor Carpi Ulnaris Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 65: Radial Nerve Block at the Wrist
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 66: Injection Technique for de Quervain Tenosynovitis
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 67: Injection Technique for Intersection Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 68: Intraarticular Injection of the Carpometacarpal Joint of the Thumb
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 69: Intraarticular Injection of the Carpometacarpal Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 70: Flexor Pollicis Longus Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 71: Flexor Digitorum Superficialis Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 72: Digital Nerve Block of the Thumb
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 73: Sesamoid Joint Injection of the Hand
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 74: Intraarticular Injection of the Metacarpophalangeal Joints
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 75: Intraarticular Injection of the Interphalangeal Joints
Indications and Clinical Syndromes
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 76: Injection Technique for Carpal Tunnel Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 77: Ulnar Nerve Block at the Wrist
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 78: Carpal Boss Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 79: Injection Technique for Secretan Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 80: Injection Technique for Os Centrale Carpi
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 81: Injection Technique for Ganglion Cysts of the Wrist and Hand
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 82: Dupuytren Contracture Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 83: Digital Nerve Block of the Finger
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Section 5: Chest Wall, Trunk, Back, and Abdomen
Chapter 84: Injection Technique for Sternoclavicular Joint Pain
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 85: Long Thoracic Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 86: Suprascapular Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 87: Costosternal Joint Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 88: Costovertebral Joint Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 89: Costosternal Joint Injection Technique for Tietze Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 90: Manubriosternal Joint Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 91: Injection Technique for Sternalis Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 92: Xiphisternal Joint Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 93: Injection Technique for Slipping Rib Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 94: Anterior Cutaneous Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 95: Injection Technique for Lumbar Myofascial PainSyndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Section 6: Hip and Pelvis
Chapter 96: Intraarticular Injection of the Hip Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 97: Adductor Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 98: Ischial Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 99: Gluteal Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 100: Psoas Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 101: Iliopectineal Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 102: Trochanteric Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 103: Injection Technique for Thigh Splints
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 104: Injection Technique for Snapping Hip Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 105: Intraarticular Injection of the Sacroiliac Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 106: Injection Technique for Gluteus Maximus Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 107: Injection Technique for Gluteus Medius Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 108: Injection Technique for Levator Ani Pain Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 109: Obturator Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 110: Lateral Femoral Cutaneous Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 111: Sciatic Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 112: Injection Technique for Osteitis Pubis Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 113: Ilioinguinal Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 114: Genitofemoral Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 115: Sacrococcygeal Joint Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Section 7: Knee and Lower Extremity
Chapter 116: Intraarticular Injection of the Knee Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 117: Superior Tibiofibular Joint Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 118: Injection Technique for Semimembranosus Insertion Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 119: Coronary Ligament Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 120: Medial Collateral Ligament Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 121: Injection Technique for Quadriceps Expansion Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 122: Quadriceps Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 123: Suprapatellar Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 124: Prepatellar Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 125: Superficial Infrapatellar Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 126: Deep Infrapatellar Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 127: Pes Anserinus Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 128: Iliotibial Band Bursa Injection
Indications and Clinical Syndromes
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 129: Medial Collateral Ligament Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 130: Iliotibial Band Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 131: Hamstring Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 132: Injection Technique for Baker Cyst
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 133: Fabella Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 134: Fascia Lata Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 135: Saphenous Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Section 8: Ankle and Foot
Chapter 136: Intraarticular Injection of the Ankle Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 137: Intraarticular Injection of the Subtalar Joint
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 138: Intraarticular Injection of the Midtarsal Joints
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 139: Intraarticular Injection of the Toe Joints
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 140: Deltoid Ligament Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 141: Anterior Talofibular Ligament Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 142: Deep Peroneal Nerve Block
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 143: Tibial Nerve Block at theAnkle
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 144: Achilles Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 145: Achilles Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 146: Fibulocalcaneal Ligament Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 147: Peroneal Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 148: Plantar Fasciitis Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 149: Injection Technique for Calcaneal Spurs
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 150: Superficial Extensor Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 151: Posterior Tibialis Tendon Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 152: Injection Technique for Bunion Pain Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 153: Injection Technique for Bunionette Pain Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 154: Injection Technique for Mallet Toe Pain Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 155: Injection Technique for Hammer Toe Pain Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 156: Injection Technique for Morton Neuroma Syndrome
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 157: Intermetatarsal Bursa Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 158: Sesamoid Bone Injection of the Foot
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Chapter 159: Metatarsal Liagament Injection
Indications and Clinical Considerations
Clinically Relevant Anatomy
Technique
Side Effects and Complications
Index
Copyright

1600 John F. Kennedy Blvd.
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ATLAS OF PAIN MANAGEMENT INJECTION TECHNIQUES    ISBN: 978-1-4377-3793-6
Copyright © 2013, 2007, 2000 by Saunders, an imprint of Elsevier Inc.
All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions .
This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notices
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the author assumes any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.
Library of Congress Cataloging-in-Publication Data
Waldman, Steven D.
 Atlas of pain management injection techniques / Steven D. Waldman. — 3rd ed.
  p. ; cm.
 Includes bibliographical references and index.
 ISBN 978-1-4377-3793-6 (hardcover : alk. paper)
 I. Title.
 [DNLM: 1. Pain—drug therapy—Atlases. 2. Injections—methods—Atlases. WL 17]
615’.6—dc23    2012012534
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Illustrator: Jennifer C. Darcy
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Dedication
To E. Grey Dimond, MD
Clinician, Educator, Visionary, Mentor, and Friend
Preface
One hundred twenty-seven years have passed since Carl Koller first used cocaine to perform an eye operation without pain. Although Koller’s landmark discovery forever changed how surgery is performed and he unwittingly created a cottage industry in regional anesthesia drugs, needles, and, of course, regional anesthesia textbooks, a careful analysis of the ensuing 127 years reveals that most of the advances in regional anesthesia drugs have centered around the development of safer local anesthetics and improved needles. The landmark texts by Pitkin, DeJong, Moore, and others helped make the use of regional anesthesia drugs accessible to the general practitioner. These early books standardized techniques, needle sizes and lengths, and, perhaps most important, the dosages of local anesthetics for the common techniques. Lofgren’s discovery of lidocaine in 1943 moved regional anesthesia drugs into the operating room and obstetric suite, as well as into doctors’ and dentists’ offices. Much safer than ester local anesthetics such as procaine, the most widely used local anesthetic up to that time, lidocaine’s larger therapeutic window was much more forgiving of clinical missteps when nerve blocks were performed, and lidocaine has been the mainstay of regional anesthesia drugs ever since.
In the 1980s, pain medicine came into its own as practitioners tested and applied the simple hypothesis that the cause of pain must be diagnosed first to ensure a successful treatment. Along with the birth of this new subspecialty came a new set of “bibles” by Raj and by Cousins and Bridenbaugh and the first edition of Atlas of Pain Management Injection Techniques, which was first published in 2000.
I think that the field of pain management is entering a new and exciting era, now that ultrasound guidance has become increasingly utilized when regional anesthesia drugs are administered. Only time will tell whether ultrasound guidance is a true “moment” or merely a passing fancy that will go the way of nesacaine and succinylcholine drips, but my clinical impression is that ultrasound guidance represents an important advance in regional anesthesia and pain management that I think will stand the test of time. In addition to presenting the fundamentals of ultrasound guidance in the how-to-do-it format that has made previous editions of this book so popular, I have included many new color figures and ultrasound, fluoroscopic, and magnetic resonance images, along with new full-color, clinically relevant anatomic drawings to make the techniques described even more accessible to my readers. With the able assistance of Sabina Borza, Content Development Specialist, we have added clear, concise captions to every figure and strived to improve the layout of the book to make it even more readable than previous editions.
I sincerely hope that you will enjoy using this book as much as I enjoyed writing it.

Steven D. Waldman, MD, JD
2012
Acknowledgments
I would like to thank my editor, Pamela Hetherington, for her wisdom, hard work, and patience and Sabina Borza, who worked tirelessly to improve the content and layout of this book.
SDW
Section 1
Head and Neck
Chapter 1 Temporomandibular Joint Injection

Indications and Clinical Considerations
Injection of the temporomandibular joint is indicated as an important component in the management of temporomandibular joint dysfunction, in the palliation of pain secondary to internal derangement of the joint, and in the treatment of pain secondary to arthritis of the joint. Temporomandibular joint dysfunction (also known as myofascial pain dysfunction of the muscles of mastication ) is characterized by pain in the joint itself that radiates into the mandible, ear, neck, and tonsillar pillars. Headache often accompanies the pain of temporomandibular joint dysfunction and is clinically indistinguishable from tension-type headache. Stress is often the precipitating or exacerbating factor in the development of temporomandibular joint dysfunction. Dental malocclusion may also play a role in the evolution of temporomandibular joint dysfunction. Internal derangement and arthritis of the temporomandibular joint may manifest as clicking or grating when the joint is opened and closed ( Figure 1-1 ). If the condition is not treated, the patient may experience increasing pain in the just-mentioned areas and limitation of jaw movement and opening. Recently the injection of autologous blood into the temporomandibular joint has gained popularity in the treatment of recurrent temporomandibular joint hypermobility dislocation ( Figure 1-2 ). This injection technique is also useful in the injection of other substances into the temporomandibular joint such as hyaluronic acid derivatives and tenoxicam.

Figure 1-1 Osteoarthritis compared in a specimen radiograph (A) and photograph (B) of a sagittally sectioned specimen. The joint space is narrow and the disk is dislocated anteriorly, with thinning and fraying of the meniscal (m) posterior attachment or bilaminar zone. The condylar head cortex is thickened, with small osteophytes (arrows). The mandibular fossa is sclerotic and remodeled, and only a shallow concavity is seen where the articular eminence once was.
(From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Figure 1-2 Injection of autologous blood into the temporomandibular joint.
(From Daif ET: Autologous blood injection as a new treatment modality for chronic recurrent temporomandibular joint dislocation, Oral Surg Oral Med Oral Pathol Oral Radiol Endod 109:31-36, 2010.)

Clinically Relevant Anatomy
The temporomandibular joint is a true joint that is divided into an upper and a lower synovial cavity by a fibrous articular disk. Internal derangement of this disk may result in pain and temporomandibular joint dysfunction, but extracapsular causes of temporomandibular joint pain are much more common. The joint space between the mandibular condyle and the glenoid fossa of the zygoma may be injected with small amounts of local anesthetic and corticosteroid. The temporomandibular joint is innervated by branches of the mandibular nerve. The muscles involved in temporomandibular joint dysfunction often include the temporalis, masseter, and external pterygoid and internal pterygoid and may include the trapezius and sternocleidomastoid. Trigger points may be identified when these muscles are palpated.

Technique
The patient is placed in the supine position with the cervical spine in the neutral position. The temporomandibular joint is identified by asking the patient to open and close his or her mouth several times and by palpating the area just anterior and slightly inferior to the acoustic auditory meatus. After the joint has been identified, the patient is asked to hold his or her mouth in a neutral position.
A total of 0.5 mL of local anesthetic is drawn up in a 3-mL sterile syringe. When temporomandibular joint dysfunction, internal derangement of the temporomandibular joint, arthritis pain of the temporomandibular joint, or other painful conditions involving the temporomandibular joint are treated, a total of 20 mg of depot corticosteroid is added to the local anesthetic with the first block, and 10 mg of depot corticosteroid is added to the local anesthetic with subsequent blocks.
After the skin overlying the temporomandibular joint has been prepared with antiseptic solution, a 25-gauge, 1-inch styletted needle is inserted just below the zygomatic arch directly in the middle of the joint space. The needle is advanced ½ to ¾ inch in a plane perpendicular to the skull until a “pop” is felt that indicates the joint space has been entered ( Figure 1-3 ). After careful aspiration, 1 mL of solution is slowly injected. Injection of the joint may be repeated at 5- to 7-day intervals if the symptoms persist.

Figure 1-3 Needle placement into the temporomandibular joint is simplified by having the patient open and close the mouth to facilitate identification of the joint.

Side Effects and Complications
This anatomic region is highly vascular. This vascularity and proximity to major blood vessels also give rise to an increased incidence of postblock ecchymosis and hematoma formation, and the patient should be warned of such. In spite of the vascularity of this anatomic region, this technique can be performed safely in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block will also decrease the amount of postprocedure pain and bleeding the patient may experience.
Additional side effects that occur with sufficient frequency include inadvertent block of the facial nerve with associated facial weakness. When this occurs, protection of the cornea with sterile ophthalmic lubricant and patching is mandatory.

Clinical Pearls
Pain from temporomandibular joint dysfunction requires careful evaluation to design an appropriate treatment plan. Infection and inflammatory causes including collagen vascular diseases first must be ruled out. When temporomandibular joint pain occurs in older patients, the pain must be distinguished from the jaw claudication associated with temporal arteritis. Stress and anxiety often accompany temporomandibular joint dysfunction; these factors must be addressed and treated. The myofascial pain component of temporomandibular joint dysfunction is best treated with tricyclic antidepressant compounds such as amitriptyline. Dental malocclusion and nighttime bruxism should be treated with an acrylic bite appliance. Narcotic analgesics and benzodiazepines should be avoided in patients with temporomandibular joint dysfunction.

Suggested Readings

Daif E.T. Autologous blood injection as a new treatment modality for chronic recurrent temporomandibular joint dislocation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod . 2010;109:31–36.
Mountziaris P.M., Kramer P.R., Mikos A.G. Emerging intra-articular drug delivery systems for the temporomandibular joint. Methods . 2009;47:134–140.
Sidebottom A.J. Current thinking in temporomandibular joint management. Br J Oral Maxillofac Surg . 2009;47:91–94.
Waldman S.D. Temporomandibular joint dysfunction. In: Pain review . Philadelphia: Saunders–Elsevier; 2009.
Waldman S.D. Temporomandibular joint injection. In: Pain review . Philadelphia: Saunders–Elsevier; 2009.
Chapter 2 Supraorbital Nerve Block

Indications and Clinical Considerations
Supraorbital nerve block is useful in the diagnosis and treatment of swimmer’s headache and supraorbital neuralgia. Swimmer’s headache is the result of compression of the supraorbital nerves by swimming goggles that fit poorly or are worn too tightly, exerting pressure on the supraorbital nerves as they exit the supraorbital foramen. Repetitive microtrauma from wearing swim goggles may also cause swimmer’s headache. The pain of swimmer’s headache is characterized as persistent pain in the supraorbital region and forehead with occasional sudden, shocklike paresthesias in the distribution of the supraorbital nerves. Sinus headache involving the frontal sinuses, which is much more common than swimmer’s headache, occasionally mimics the pain of swimmer’s headache. Occasionally, a patient with swimmer’s headache will complain that the hair on the front of the head “hurts.”

Clinically Relevant Anatomy
The supraorbital nerve arises from fibers of the frontal nerve, which is the largest branch of the ophthalmic nerve. The frontal nerve enters the orbit via the superior orbital fissure and passes anteriorly beneath the periosteum of the roof of the orbit. The frontal nerve gives off a larger lateral branch, the supraorbital nerve, and a smaller medial branch, the supratrochlear nerve. Both exit the orbit anteriorly. The supraorbital nerve sends fibers all the way to the vertex of the scalp and provides sensory innervation to the forehead, upper eyelid, and anterior scalp ( Figure 2-1 ).

Figure 2-1 Swimmer’s headache is characterized by persistent pain in the supraorbital region with associated intermittent shocklike paresthesias.

Technique
The patient is placed in a supine position. A total of 3 mL of local anesthetic is drawn up in a 10-mL sterile syringe. When swimmer’s headache is treated with supraorbital nerve block, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks.
The supraorbital notch on the affected side is then identified by palpation. The skin overlying the notch is prepared with antiseptic solution, with care being taken to avoid spillage into the eye. A 25-gauge, 1½-inch needle is inserted at the level of the supraorbital notch and is advanced medially approximately 15 degrees off the perpendicular to avoid entering the foramen. The needle is advanced until it approaches the periosteum of the underlying bone ( Figure 2-2 ). A paresthesia may be elicited, and the patient should be warned of such. The needle should not enter the supraorbital foramen; should this occur, the needle should be withdrawn and redirected slightly more medially.

Figure 2-2 When the needle is placed for supraorbital nerve block, care should be taken to avoid advancing the needle into the supraorbital foramen.
Because of the loose alveolar tissue of the eyelid, a gauze sponge should be used to apply gentle pressure on the upper eyelid and supraorbital tissues before injection of solution to prevent the injectate from dissecting inferiorly into these tissues. This pressure should be maintained after the procedure to avoid periorbital hematoma and ecchymosis.
After gentle aspiration, 3 mL of solution is injected in a fanlike distribution. If blockade of the supratrochlear nerve is also desired, the needle is then redirected medially; after careful aspiration, an additional 3 mL of solution is injected in a fanlike manner.

Side Effects and Complications
The forehead and scalp are highly vascular, and the pain specialist should carefully calculate the total milligram dose of local anesthetic that may be safely given, especially if bilateral nerve blocks are being performed. This vascularity gives rise to an increased incidence of postblock ecchymosis and hematoma formation. In spite of the vascularity of this anatomic region, this technique can be safely performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls
Supraorbital nerve block is especially useful in the diagnosis and palliation of pain secondary to swimmer’s headache and supraorbital neuralgia. The first step in the management of the unusual cause of headache is the correct fitting of swim goggles that do not compress the supraorbital nerves. Coexistent frontal sinusitis should be ruled out in patients who do not respond rapidly to a change in swim goggles and a series of the just-described nerve blocks.
Any patient with headaches severe enough to require neural blockade as part of the treatment plan should undergo computed tomography (CT) or magnetic resonance imaging (MRI) of the head to rule out unsuspected intracranial pathology.

Suggested Readings

Levin M. Nerve blocks in the treatment of headache. Neurotherapeutics . 2010;7:197–203.
O’Brien J.C., Jr. Swimmer’s headache, or supraorbital neuralgia. Proc (Bayl Univ Med Cent) . 2004;17:418–419.
Pareja J.A., Caminero A.B. Supraorbital neuralgia. Curr Pain Headache Rep . 2006;10:302–305.
Sharma R.R., Pawar S.J., Lad S.D., et al. Frontal intraosseous cryptic hemangioma presenting with supraorbital neuralgia. Clin Neurol Neurosur . 1999;101:215–219.
Sjaastad O., Stolt-Nielsen A., Pareja J.A., et al. Supraorbital neuralgia. On the clinical manifestations and a possible therapeutic approach. Headache . 1999;39:204–212.
Chapter 3 Trochlear Nerve Block

Indications and Clinical Considerations
Trochlear injection is useful in the diagnosis and treatment of primary trochlear headache. As with most headache syndromes, the exact cause of the pain of primary trochlear headache is unknown, and whether the trochlear nerve plays a role in pathogenesis of this uncommon source of head and face pain is the subject of ongoing debate.
In patients with primary trochlear headache the presenting symptom is unilateral periorbital pain radiating from the trochlear area with associated headache. The pain of primary trochlear headache is exacerbated by supraduction of the affected eye, although no limitation of range of motion of the superior oblique should be noted. The pain of this uncommon headache syndrome is often worse at night, and whereas initially the pain is characterized by remissions and exacerbations, without treatment it can become chronic. As the name implies, primary trochlear headache is a diagnosis of exclusion because it occurs in the absence of primary orbital, retro-orbital, or ocular pathology.
Often confused with acute ocular diseases such as glaucoma or herpes zoster of the first division of the trigeminal nerve or Charlin syndrome, pathology of the orbit and the retro-orbital region must be ruled out before the diagnosis of primary trochlear headache can be made. Inflammatory and autoimmune conditions involving the trochlear nerve anywhere along its path such as multiple sclerosis, cranial neuritis, and Tolosa-Hunt syndrome, as well as compromise of the trochlear nerve by tumor, abscess, or vascular abnormality must be carefully sought before the diagnosis of primary trochlear can be considered ( Figures 3-1 and 3-2 ). The diagnosis of primary trochlear headache is then confirmed by injection of the trochlear region with local anesthetic and antiinflammatory steroid. Primary trochlear headache will uniformly respond to this injection.

Figure 3-1 Axial, T1-weighted, contrast-enhanced image demonstrates soft tissue in the left cavernous sinus, which has enhanced markedly. The enhancement extends along the free edge of the tentorium cerebelli. Imaging is nonspecific, but after exclusion of other conditions this patient was diagnosed with Tolosa-Hunt syndrome.
(From Tang Y, Booth T, Steward M, et al: The imaging of conditions affecting the cavernous sinus, Clin Radiol 65:937-945, 2010.)

Figure 3-2 Axial T1-weighted image with gadolinium and fat saturation. This 55-year-old man had painful ophthalmoplegia (III, IV, VI, and VI) and slight proptosis of the right eye. Magnetic resonance imaging shows an enhancing ill-defined process in the right orbital apex. Cavernous sinus not involved (Tolosa-Hunt syndrome).
(From Ferreira T, Verbist B, van Buchem M, et al: Imaging the ocular motor nerves, Eur J Radiol 74:314-322, 2010.)

Clinically Relevant Anatomy
The trochlear nerve (cranial nerve IV) is composed of somatic general efferent motor fibers. It innervates the superior oblique extraocular muscle of the contralateral orbit ( Figure 3-3 ). Contraction of the superior oblique extraocular muscle intorts (rotates inward), depresses, and abducts the globe. The superior oblique extraocular muscle works in concert with the five other extraocular muscles to allow the eye to perform its essential functions of tracking and fixation on objects.

Figure 3-3 Trochlear nerve (IV) in the orbit.
(From Drake RL, Vogl W, Mitchell AWM: Gray’s anatomy for students, ed 2, Philadelphia, 2010, Churchill Livingstone.)
The fibers of the trochlear nerve originate from the trochlear nucleus, which is just ventral to the cerebral aqueduct in the tegmentum of the midbrain at the level of the inferior colliculus. As the trochlear nerve leaves the trochlear nucleus, it travels dorsally, wrapping itself around the cerebral aqueduct to then decussate in the superior medullary velum. The decussated fibers of the trochlear nerve then exit the dorsal surface of the brainstem just below the contralateral inferior colliculus, where they then curve around the brainstem, leaving the subarachnoid space along with the oculomotor nerve (cranial nerve III) between the superior cerebellar and posterior cerebral arteries. The trochlear nerve then enters the cavernous sinus and runs anteriorly along the lateral wall of the sinus with the oculomotor nerve (cranial nerve III), trigeminal nerve (cranial nerve V), and abducens nerve (cranial nerve VI).
After exiting the cavernous sinus, the trochlear nerve enters the orbit via the superior orbital fissure. Unlike the oculomotor nerve, the trochlear nerve does not pass through the tendinous ring of the extraocular muscles but passes just above the ring. The trochlear nerve then crosses medially along the roof of the orbit above the levator palpebrae and superior rectus muscles to innervate the superior oblique muscle (see Figure 3-3 ).
Disorders of the trochlear nerve can be caused by central lesions that affect the trochlear nucleus such as stroke or space-occupying lesions such as tumor, abscess, or aneurysm. Increased intracranial pressure from subdural hematoma, sagittal sinus thrombosis, or abscess can compromise the nucleus and/or the efferent fibers of the trochlear nerve as they exit the brainstem and travel toward the orbit, with resultant abnormal nerve function. Traction on the trochlear nerve from loss of cerebrospinal fluid has also been implicated in cranial nerve IV palsy. Small vessel disease from diabetes or vasculitis associated with temporal arteritis may cause ischemia and even infarction of the trochlear nerve with resultant pathologic symptoms.
In almost all disorders of the trochlear nerve, symptoms will take the form of a palsy of the superior oblique muscle, most commonly manifesting as an inability to look inward and downward. Often the patient will report difficulty in walking down stairs owing to the inability to depress the affected eye or eyes. On physical examination the clinician may note extorsion (outward rotation) of the affected eye as a result of the unopposed action of the inferior oblique muscle ( Figure 3-4 , A ). In an effort to compensate, the patient may deviate his or her face forward and downward with the chin rotated toward the affected side to look downward ( Figure 3-4 , B ). However, it should be remembered that isolated trochlear nerve palsy is the least common of the ocular motor palsies, and its presence should be viewed as an ominous warning sign.

Figure 3-4 A, The unopposed action of the inferior oblique muscle in the presence of trochlear nerve palsy results in extorsion of the globe and associated weak downward gaze. B, To compensate for the unopposed action of the inferior oblique muscle in the presence of trochlear palsy, the patient deviates his face forward and downward with the chin rotated toward the affected side.

Technique
The patient is placed in a supine position. A total of 2 mL of local anesthetic is drawn up in a 10-mL sterile syringe. When primary trochlear headache is treated with trochlear region block, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks.
For trochlear region block to be performed, the medial canthus is identified and a line is drawn superiorly to a point just below the eyebrow. The skin at the midpoint of this line is prepared with antiseptic solution, with care being taken to avoid spillage into the eye. A 25-gauge, 1½-inch needle is inserted at this point and advanced until the tip of the needle makes contact with the bony surface of the orbit. After careful gentle aspiration, the contents of the syringe are slowly injected as the needle is slowly directed superiorly and inferiorly ( Figure 3-5 ). Because of the loose alveolar tissue of the eyelid, a gauze sponge should be used to apply gentle pressure on the upper eyelid and supraorbital tissues before injection of solution to prevent the injectate from dissecting inferiorly into these tissues. This pressure should be maintained after the procedure to avoid periorbital hematoma and ecchymosis. When trochlear region block is used to treat the pain and symptoms associated with primary trochlear headache, 8 to 10 daily nerve blocks with local anesthetic may be required. If daily blocks are being performed, as a general rule the total dose of depot corticosteroids included in these blocks should not exceed 360 to 400 mg.

Figure 3-5 For trochlear block to be performed, the medial canthus is identified, and a line is drawn superiorly to a point just below the eyebrow.

Side Effects and Complications
The major complication of this procedure is inadvertent injury to the eye. Failure to maintain bony contact while advancing the needle will greatly increase the risk of the devastating complication. The practitioner should also remember that this area is highly vascular and the potential for intravascular injection of local anesthetic with its attendant risks remains an ever-present possibility. This vascularity gives rise to an increased incidence of postblock ecchymosis and hematoma formation. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding.

Clinical Pearls
Trochlear nerve block is especially useful in the diagnosis and palliation of pain secondary to primary trochlear headache. The first step in the care of patients thought to have this unusual cause of headache is ruling out more common types of headache that may mimic primary trochlear headache. Any patient with headaches bad enough to require neural blockade as part of the treatment plan should undergo computed tomography (CT) or magnetic resonance imaging (MRI) of the head to rule out unsuspected intracranial pathologic conditions.

Suggested Readings

Becker M., Kohler R., Vargas M.I., et al. Pathology of the trigeminal nerve. Neuroimaging Clin N Am . 2008;18:283–307.
Ferreira T., Verbist B., van Buchem M., et al. Imaging the ocular motor nerves. Eur J Radiol . 2010;74:314–322.
Lin C.M., Hseu I.H. Isolated trochlear nerve palsy associated with carotid-cavernous sinus fistula. Int J Gerontol . 2009;3:129–132.
Rait J. Ocular causes of headache. In: Selvaratnam P., Niere K., Zuluaga M. Headache, orofacial pain and bruxism . New York: Churchill Livingstone; 2009:127–138.
Waldman S.D. The trochlear nerve—cranial nerve IV. In: Pain review . Philadelphia: Saunders–Elsevier; 2009.
Yangüela J., Sánchez-del-Rio M., Bueno A., et al. Primary trochlear headache: a new cephalgia generated and modulated on the trochlear region. Am J Ophthalmol . 2004;138:703.
Yangüela J., Sánchez-del-Rio M., Bueno A., et al. Primary trochlear headache: a new cephalgia generated and modulated on the trochlear region. Neurology . 2004;62:1134–1140.
Chapter 4 Buccal Fold Injection for Incisors and Canine Teeth

Indications and Clinical Considerations
The buccal fold injection technique is useful in the diagnosis and treatment of pain involving the incisors or canine teeth of the upper jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin.
Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, and tooth extractions ( Figure 4-1 ). Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis.

Figure 4-1 Intruded primary incisor. A, Day of injury. B, Radiograph on day of injury. C, Three weeks postinjury. D, Five months postinjury.
(From McTigue DJ: Managing injuries to the primary dentition, Dent Clin North Am 53:627-638, 2009.)
Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Clinically Relevant Anatomy
The incisor and canine and surrounding periosteum and buccal and gingival tissue are innervated by the superior alveolar nerve, which is a branch of the inferior alveolar nerve just before it exits from the infraorbital canal below the orbit ( Figure 4-2 ). Fibers of the ipsilateral superior alveolar nerve may cross the midline and may anastomose with fibers of the contralateral nerve, although medial spread of injected local anesthetics may be limited by the attachments of the labial frenulum at the midline. The periosteum and bone that surround and support the root of the tooth are relatively thin and readily allow diffusion of local anesthetics injected in this region ( Figure 4-3 ).

Figure 4-2 The relationship of the superior alveolar nerve to the incisor and canine.

Figure 4-3 Lateral view of the canine demonstrating relationship of the supporting structures and apical region.

Technique
The patient is placed in a supine position. A total of 1 to 2 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The lip overlying the affected tooth is retracted, and a small amount of topical anesthetic such as viscous lidocaine or EMLA cream is applied to the alveolar sulcus with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, 1½-inch needle is inserted through the previously anesthetized area and advanced axially and slightly medially toward the apex of the affected tooth. When the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration the local anesthetic is slowly injected around the apex target area. The anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth ( Figure 4-4 ). It should be remembered that the root of the canine tooth is longer than the root of the incisor and the apical portion of the root is often slightly more distally oriented.

Figure 4-4 Proper needle placement with needle tip in good position. Green area indicates the initial flow of local anesthetic.

Side Effects and Complications
In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic resulting from placement that is too superficial or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain from overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls
Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.


Suggested Readings

Abt E. Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection. J Evid Based Dent Pract . 2010;10:160–161.
Kato T., Lavigne G.J. Sleep bruxism: a sleep-related movement disorder. Sleep Med Clin . 2010;5:9–35.
McTigue D.J. Managing injuries to the primary dentition. Dent Clin North Am . 2009;53:627–638.
van Wijk A.J., Hoogstraten J. Anxiety and pain during dental injections. J Dent . 2009;37:700–704.
Zadik Y. Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod . 2010;109:e65–e69.
Zadik Y., Vainstein V., Heling I., et al. Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain. J Endod . 2010;36:1588–1592.
Chapter 5 Buccal Fold Injection Technique for Upper Premolar Teeth

Indications and Clinical Considerations
The buccal fold injection technique is useful in the diagnosis and treatment of pain involving the premolar teeth of the upper jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin.
Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, and tooth extraction. Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis.
Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Clinically Relevant Anatomy
The upper premolar is innervated by the superior dental plexus, which is composed of convergent fibers from the superior, posterior, and anterior alveolar nerves ( Figure 5-1 ). In some patients the premolars are innervated from fibers from the middle superior alveolar nerve. The periosteum and bone that surround and support the root of the tooth are relatively thin and readily allow diffusion of local anesthetics injected in this region ( Figure 5-2 ). The adjacent palate is innervated by the greater palatine nerve and occasionally fibers of the nasopalatine nerve ( Figure 5-3 ). Supplemental blockade of these nerves will often be required to completely relieve upper premolar pain.

Figure 5-1 Innervation of the upper premolars.

Figure 5-2 Spread of local anesthetic with blockade of upper premolar. Green indicates spread of local anesthetic.

Figure 5-3 Anatomy of the greater palatine nerve.

Technique
The patient is placed in a supine position. A total of 1 to 2 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The lip overlying the affected tooth is retracted, and a small amount of topical anesthetic such as viscous lidocaine or EMLA cream is applied to the alveolar sulcus with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, 1½-inch needle is inserted through the previously anesthetized area and advanced axially toward the apex of the affected tooth ( Figure 5-4 ). If the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration the local anesthetic is slowly injected around the apex target area. The anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth. Supplemental block of the greater palatine nerve is carried out by placing the needle at right angles to the mucosa at a point approximately half the height of the affected premolar ( Figure 5-5 ).

Figure 5-4 Needle placement for block of the upper premolars.

Figure 5-5 Needle placement for greater palatine nerve block.

Side Effects and Complications
In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic as a result of placement that is too superficial placement or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain caused by overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls
Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

Suggested Readings

Abt E. Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection. J Evid Based Dent Pract . 2010;10:160–161.
Kato T., Lavigne G.J. Sleep bruxism: a sleep-related movement disorder. Sleep Med Clin . 2010;5:9–35.
McTigue D.J. Managing injuries to the primary dentition. Dent Clin North Am . 2009;53:627–638.
van Wijk A.J., Hoogstraten J. Anxiety and pain during dental injections. J Dent . 2009;37:700–704.
Zadik Y. Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod . 2010;109:e65–e69.
Zadik Y., Vainstein V., Heling I., et al. Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain. J Endod . 2010;36:1588–1592.
Chapter 6 Buccal Fold Injection for Upper Molar Teeth

Indications and Clinical Considerations
The buccal fold injection technique is useful in the diagnosis and treatment of pain involving the molars of the upper jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin.
Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, and tooth extraction. Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis.
Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Clinically Relevant Anatomy
The upper molars and surrounding periosteum and buccal and gingival tissue are innervated by the superior alveolar nerve, which branches from the infraorbital nerve before it enters the orbital cavity. These branches travel downward along the maxillary tuberosity to provide innervation for the upper molars and the buccal gingiva and associated periosteum. The gingiva, mucosa, and periosteum of the adjacent palate are innervated by the greater palatine nerve ( Figure 6-1 ). The greater palatine nerve passes from the pterygopalatine fossa via the pterygopalatine canal through the pterygopalatine foramen (see Figure 5-3 ). In some patients an anatomic variation occurs, and the upper molars are innervated primarily by the middle alveolar nerves. This variation has little clinical import insofar as the success of this block is concerned. The palate adjacent to the molars is innervated by the greater palatine nerve and in some patients by small anastomosing branches of the nasopalatine nerve (see Figure 5-3 ). The periosteum and bone that surround and support the roots of the molars are relatively thin and readily allow diffusion of local anesthetics injected in this region. For satisfactory anesthesia to be provided to the upper molars, three separate injections are usually required: (1) the buccal fold injection, (2) the tuberosity injection, and (3) the supplemental greater palatine nerve injection. Each injection is described in the following sections.

Figure 6-1 Innervation of the upper molars.

Technique

Buccal Fold Injection
The patient is placed in a supine position. If the more distal molars are to be blocked, it is important not to have the patient open the mouth too widely, or the coronoid process of the mandible will move ventrally and block the injection site. A total of 4 mL of local anesthetic is drawn up in a 5-mL sterile syringe. The lip overlying the affected tooth is retracted, and a small amount of topical anesthetic such as viscous lidocaine or EMLA cream is applied to the alveolar sulcus with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, 1½-inch needle is inserted through the previously anesthetized area and advanced axially and slightly posteriorly toward the apex of the affected tooth. When the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration 1 to 2 mL of local anesthetic is slowly injected around the apex target area; the anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth ( Figures 6-2 and 6-3 ). It should be noted that unlike the previously described buccal fold injection techniques for the incisors, canines, and premolars, this technique yields relatively little anesthesia of the adjacent lip ( Figure 6-4 ).

Figure 6-2 Buccal fold injection for the upper molars.

Figure 6-3 Needle trajectory for buccal fold injection for the upper molars.

Figure 6-4 Spread of anesthesia after buccal fold injection for the upper molars. Note the relative lack of lip anesthesia.

Tuberosity Injection
The lip overlying the affected tooth is retracted, and the infrazygomatic crest is palpated with the gloved index finger, which also gently retracts the corner of the mouth posteriorly. A 25-gauge, 1½-inch needle is inserted slightly distal to the second molar and; while it is kept close to the maxillary tuberosity, it is advanced in a superior and posterior trajectory ( Figure 6-5 ). After gentle aspiration, an additional 2 mL of local anesthetic is slowly injected around the apex target area; the anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth ( Figure 6-6 ). This injection will augment the anesthesia of the second and third molars ( Figure 6-7 ).

Figure 6-5 Tuberosity injection for the upper molars.

Figure 6-6 Needle trajectory for tuberosity injection for the upper molars.

Figure 6-7 Spread of anesthesia after tuberosity injection for the upper molars.

Supplemental Greater Palatine Nerve Injection
Most patients with significant molar pain or those undergoing major procedures on the molars (e.g., root canals, extractions) will require supplementation of the anesthesia, obtained with upper molar dental block with injection of the fibers of the greater palatine nerve. This technique is carried out through injection of 0.1 to 0.2 mL of local anesthetic at right angles to the affected tooth at a point approximately one half of the tooth height ( Figures 6-8 and 6-9 ).

Figure 6-8 Injection of the greater palatine nerve for anesthesia of the upper molars.

Figure 6-9 Spread of anesthesia after greater palatine nerve injection for the upper molars.

Side Effects and Complications
In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic as a result of placement that is too superficial placement or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain caused by overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls
Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

Suggested Reading

Abt E. Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection. J Evid Based Dent Pract . 2010;10:160–161.
Kato T., Lavigne G.J. Sleep bruxism: a sleep-related movement disorder. Sleep Med Clin . 2010;5:9–35.
McTigue D.J. Managing injuries to the primary dentition. Dent Clin North Am . 2009;53:627–638.
Mylonas A.I., Tzerbos F.H., Mihalaki M., et al. Cerebral abscess of odontogenic origin. J Craniomaxillofac Surg . 2007;35:63–67.
van Wijk A.J., Hoogstraten J. Anxiety and pain during dental injections. J Dent . 2009;37:700–704.
Zadik Y. Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod . 2010;109:e65–e69.
Zadik Y., Vainstein V., Heling I., et al. Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain. J Endod . 2010;36:1588–1592.
Chapter 7 Incisive Nerve Block

Indications and Clinical Considerations
This injection technique is useful in the diagnosis and treatment of pain involving the incisors or canine teeth of the lower jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin.
Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, and tooth extraction ( Figure 7-1 ). Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis.

Figure 7-1 Right lower gingival carcinoma in a 45-year-old man with histopathologically confirmed alveolar bone invasion ( A, arrow ). A, Cropped panoramic image. B to D, Cone-beam computed tomography (CT) images ( B, horizontal; C, parallel; D, cross section). Cone-beam CT images reveal alveolar bone destruction of the right mandible ( B, C, and D, arrow ), whereas corresponding bone destruction cannot be seen on panoramic image.
(From Momin MA, Okochi K, Watanabe H, et al: Diagnostic accuracy of cone-beam CT in the assessment of mandibular invasion of lower gingival carcinoma: comparison with conventional panoramic radiography, Eur J Radiol 72:75-81, 2009.)
Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Clinically Relevant Anatomy
The lower incisors and canine teeth are innervated by a branch of the incisive nerve, which is a distal branch of the inferior dental nerve. In most patients the nerve is covered by a thin layer of osseous lamina that allows easy diffusion of local anesthetic ( Figure 7-2 ). Occasionally the bone is too thick to allow rapid diffusion of local anesthetic, and a mental or mandibular nerve block will be required. It should be noted that fibers of the contralateral incisive nerve may cross the midline and confuse the clinical picture. The buccal soft issues in this region are innervated by branches of the mental nerve, whereas the lingual gingiva and associated periosteum are innervated by branches of the sublingual nerve ( Figure 7-3 ). Supplemental blockade of the mental and sublingual nerves may be required to provide complete anesthesia for the lower incisors and canine teeth.

Figure 7-2 The incisive nerve provides innervations to the lower incisors and canines.

Figure 7-3 The relationship of the lingual nerve to the lower incisors and canines.

Technique
The patient is placed in a supine position. A total of 1 to 2 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The lip overlying the affected tooth is retracted, and a small amount of topical anesthetic such as viscous lidocaine or EMLA cream is applied to the buccal fold with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, 1½-inch needle is inserted through the previously anesthetized area and advanced toward the apex of the affected tooth. When the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration the local anesthetic is slowly injected around the apex target area; the anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth ( Figure 7-4 ). To perform the supplemental lingual nerve block, the needle is advanced just under the attached gingiva; after careful aspiration, 1.0 mL of local anesthetic is slowly injected ( Figure 7-5 ).

Figure 7-4 Buccal fold injection for the lower incisors and canine teeth.

Figure 7-5 Lingual nerve block for lower incisor and canine tooth dental pain.

Side Effects and Complications
In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic from placement that is too superficial or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain from overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergent incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls
Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

Suggested Readings

Abt E. Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection. J Evid Based Dent Pract . 2010;10:160–161.
Kato T., Lavigne G.J. Sleep bruxism: a sleep-related movement disorder. Sleep Med Clin . 2010;5:9–35.
McTigue D.J. Managing injuries to the primary dentition. Dent Clin North Am . 2009;53:627–638.
van Wijk A.J., Hoogstraten J. Anxiety and pain during dental injections. J Dent . 2009;37:700–704.
Zadik Y. Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod . 2010;109:e65–e69.
Zadik Y., Vainstein V., Heling I., et al. Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain. J Endod . 2010;36:1588–1592.
Chapter 8 Inferior Alveolar Nerve Block for Lower Premolar Teeth

Indications and Clinical Considerations
The inferior alveolar nerve block is useful in the diagnosis and treatment of pain involving the premolars of the lower jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin.
Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, or tooth extraction. Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis.
Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Clinically Relevant Anatomy
The lower premolars are innervated primarily by the inferior alveolar nerve ( Figure 8-1 ). Fibers of the buccal nerve innervate the buccal gingiva; the lingual gingiva is innervated by the sublingual nerve. Because of the thicker mandibular bone which supports the premolars, diffusion of local anesthetic with the buccal fold block is limited, and mental or mandibular nerve block is required. The mental foramen lies just inferior to and between the lower premolars ( Figure 8-2 ).

Figure 8-1 The lower premolars are innervated primarily by branches of the inferior alveolar nerve. Note the dense mandibular bone surrounding the premolars as well as the relationship of the mental foramen to the premolars.

Figure 8-2 The relationship of the mental nerve to the premolars.

Technique
The patient is placed in a supine position. A total of 1 to 2 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The mental foramen is identified, and the lower lip overlying the lower premolars is retracted. A small amount of topical anesthetic such as viscous lidocaine or EMLA cream is then applied to the alveolar sulcus just superior to the mental foramen with a cotton-tipped applicator. After topical anesthesia has been achieved, a 25-gauge, 1½-inch needle is inserted through the previously anesthetized area and advanced toward the mental foramen ( Figure 8-3 ). Care should be taken to avoid inserting the needle directly into the mental foramen to avoid inadvertent injection into the blood vessels or damage to the mental nerve. When the needle tip impinges on bone, it is withdrawn slightly out of the periosteum, and after gentle aspiration the local anesthetic is slowly injected around the apex target area; the anesthetic will rapidly diffuse and anesthetize the pulp of the affected tooth ( Figure 8-4 ). Some spillover of local anesthetic may result in blockade of some fibers of the buccal nerve, resulting in large areas of anesthesia of the buccal soft tissues. Supplemental blockade of the lingual nerve is often required to provide complete anesthesia of the premolars. To block the lingual nerves, simply place the needle just beneath the surface of the lingual mucosa adjacent to the affect premolar. After careful aspiration, 0.5 mL of local anesthetic per premolar is injected ( Figures 8-5 and 8-6 ).

Figure 8-3 Mental nerve block for lower premolar dental pain.

Figure 8-4 Area of anesthesia after mental nerve block.

Figure 8-5 Relationship of the lingual nerve to the lower premolars.

Figure 8-6 Lingual nerve block for the premolars.

Side Effects and Complications
In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic because placement is too superficial or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain caused by overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls
Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergent dental care.

Suggested Readings

Abt E. Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection. J Evid Based Dent Pract . 2010;10:160–161.
Kato T., Lavigne G.J. Sleep bruxism: a sleep-related movement disorder. Sleep Med Clin . 2010;5:9–35.
McTigue D.J. Managing injuries to the primary dentition. Dent Clin North Am . 2009;53:627–638.
van Wijk A.J., Hoogstraten J. Anxiety and pain during dental injections. J Dent . 2009;37:700–704.
Zadik Y. Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod . 2010;109:e65–e69.
Zadik Y., Vainstein V., Heling I., et al. Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain. J Endod . 2010;36:1588–1592.
Chapter 9 Inferior Alveolar Nerve Block for Lower Molar Teeth

Indications and Clinical Considerations
The inferior alveolar nerve block is useful in the diagnosis and treatment of pain involving the molars of the lower jaw. This technique can provide much-needed emergency relief of dental pain while the patient is waiting for definitive dental treatment. It can also serve as a useful diagnostic maneuver when the clinician is trying to localize the nidus of pain that the patient perceives as dental in origin.
Dental pain is the result of irritation or inflammation of the nerves of the pulp and/or root of the tooth. Common causes of irritation or inflammation responsible for dental pain include infection, decay with resultant nerve exposure, gingival disease, plaque at or below the gum line, bruxism, injury, tumor, or tooth extraction. Less common causes include chemotherapy-induced odontalgia and barodontalgia. Pain involving the incisors or canine teeth may also be referred from other anatomic areas. Such referred pain may be indicative of temporomandibular joint dysfunction, sinus disease, abnormalities of the trigeminal nerve and its branches, and coronary artery stenosis.
Dental pain may range from a dull ache to severe, unremitting pain. Its onset may be insidious or acute. Dental pain is often worse when the affected tooth or teeth are exposed to hot or cold temperatures as well as when direct pressure is applied to the tooth or teeth when chewing. Tapping on the affected tooth or teeth may elicit an acute exacerbation of the pain. If significant inflammation or infection is present, rubor and color may be present, as well as swelling. Gingival bleeding or purulent drainage may also be present. It should be remembered that on occasion a severely compromised tooth that is causing a patient significant pain may appear completely normal.

Clinically Relevant Anatomy
The lower molars are innervated primarily by the mandibular (inferior alveolar) nerve ( Figure 9-1 ). Because of the thicker mandibular bone which supports the premolars, diffusion of local anesthetic with buccal fold block is limited, and blockade of the mandibular nerve before it enters the mandibular canal is required ( Figure 9-2 ), The lingual gingiva in the region of the lower molars is innervated by the lingual nerve (see Figure 9-2 ). Terminal branches of the buccal nerve pass through the buccinator muscles and provide innervations for the buccal mucosa in the region of the lower molars (see Figure 9-2 ). For satisfactory anesthesia to be provided to the lower molars, both the mandibular and lingual nerves need to be blocked, as well as the buccal nerve ( Figure 9-3 ).

Figure 9-1 Anatomy of the mandibular nerve and lower molars.

Figure 9-2 Anatomy of the mandibular nerve and its relationship to the lingual and buccal nerves.

Figure 9-3 Relationship of the mandibular lingual and buccal nerves.

Technique
Both the mandibular and lingual nerves can be blocked with one needle stick and minor repositioning of the needle. For the mandibular and lingual nerves to be blocked, the patient is placed in a supine position and a total of 3 mL of local anesthetic is drawn up in a 3-mL sterile syringe. The patient is then asked to open his or her mouth widely, and the coronoid notch is palpated with the index finger of the left hand ( Figure 9-4 ). The syringe with an attached 25-gauge, 1½-inch needle is then directed from between the contralateral premolars toward an area approximately 1 cm above the level of the occlusal surface of the molars to be blocked just in front of the palpating index finger ( Figure 9-5 ). The patient is then asked to slightly close his or her mouth to decrease tension of the pterygoid muscles. With the decrease of tension on the tightly stretched pterygoid muscles, the lateral margin of the pterygoid muscle relaxes, allowing the displaced nerve to return to its proper anatomic position .

Figure 9-4 Palpating the coronoid notch.

Figure 9-5 Injection site for mandibular nerve block lies at the level of the finger palpating the coronoid notch, which is approximately 1 cm above the occlusal surfaces of the lower molars.
The needle is now advanced dorsally approximately 1.5 to 2.0 cm along the medial aspect of the mandibular ramus, with the trajectory of needle advancement horizontal to the occlusal plane of the molars ( Figure 9-6 ). When the needle impinges onto the middle portion of the mandibular ramus, it is withdrawn slightly, and after careful aspiration 1.5 mL of local anesthetic is injected. The needle is then withdrawn into the soft tissue and the trajectory is redirected medially and ventrally toward the mandibular crest to block the lingual nerve ( Figure 9-7 ). The buccal nerve is then blocked by inserting the needle just above the buccal fold at the third molar and advancing it toward the ipsilateral mandibular ramus ( Figure 9-8 ). After careful aspiration, 0.5 mL of additional local anesthetic is then slowly injected.

Figure 9-6 Advancement of the needle for mandibular nerve block with the needle shaft in contact with the mandibular ramus and the trajectory in the horizontal plane of the occlusal surfaces of the molars being blocked.

Figure 9-7 Needle trajectory for lingual nerve block for lower molar dental pain.

Figure 9-8 Needle trajectory for buccal nerve injection for lower molar dental pain.

Side Effects and Complications
In general, the use of nerve blocks in dentistry has enjoyed an amazing track record of utility and safety. Most side effects and complications are related to inadvertent intravascular injection, the use of local anesthetics containing epinephrine, and vasovagal syncope. Occasional hematoma and ecchymosis formation after dental nerve block is encountered, especially in patients taking anticoagulants or antiplatelet drugs. Pitfalls in needle placement include decreased diffusion of local anesthetic caused by placement that is too superficial or positioning of the needle tip between the relatively impermeable fascia and labial muscle. Excessive pain from overly rapid injection of local anesthetic should also be avoided. The clinician is reminded that severe dental abscess can be life-threatening, and emergency incision and drainage combined with aggressive antibiotic therapy may be required to avoid disaster. Referred pain as well as pain from tumor should always be considered when evaluating a patient with dental pain.

Clinical Pearls
Traumatic or nontraumatic dental pain is an increasingly frequent reason for adult and pediatric patients to visit urgent care and emergency room facilities. Often, urgent care or emergency room physicians have little or no training in the treatment of painful dental conditions. The use of dental nerve blocks with long-acting local anesthetics can provide excellent palliation of pain while the patient waits to obtain emergency dental care.


Suggested Readings

Abt E. Topical anesthetics are more effective in diminishing pain from needle stick insertion alone compared to reducing pain from insertion with anesthetic injection. J Evid Based Dent Pract . 2010;10:160–161.
Kato T., Lavigne G.J. Sleep bruxism: a sleep-related movement disorder. Sleep Med Clin . 2010;5:9–35.
McTigue D.J. Managing injuries to the primary dentition. Dent Clin North Am . 2009;53:627–638.
Mylonas A.I., Tzerbos F.H., Mihalaki M., et al. Cerebral abscess of odontogenic origin. J Craniomaxillofac Surg . 2007;35:63–67.
van Wijk A.J., Hoogstraten J. Anxiety and pain during dental injections. J Dent . 2009;37:700–704.
Zadik Y. Barodontalgia: what have we learned in the past decade? Oral Surg Oral Med Oral Pathol Oral Radiol Endod . 2010;109:e65–e69.
Zadik Y., Vainstein V., Heling I., et al. Cytotoxic chemotherapy-induced odontalgia: a differential diagnosis for dental pain. J Endod . 2010;36:1588–1592.
Chapter 10 Styloid Process Injection

Indications and Clinical Considerations
Eagle syndrome (also known as stylohyoid syndrome ) is caused by pressure on the internal carotid artery and surrounding structures including branches of the glossopharyngeal nerve by an abnormally elongated styloid process or a calcified stylohyoid ligament ( Figure 10-1 ). The pain of Eagle syndrome is sharp and stabbing and occurs with movement of the mandible or with turning of the neck. The pain starts below the angle of the mandible and radiates into the tonsillar fossa, the temporomandibular joint, and the base of the tongue. A trigger point may be present in the tonsillar fossa. Injection of the attachment of the stylohyoid ligament to the styloid process with local anesthetic and corticosteroid serves as both a diagnostic and a therapeutic maneuver. Rarely, the elongated styloid process or calcified stylohyoid ligament may actually cause vascular occlusion ( Figure 10-2 ).

Figure 10-1 Ossification of the stylohyoid ligament (Eagle syndrome). Note the large ossified structure (arrows), which represents an elongated styloid process or ossified stylohyoid ligament or both.
(From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Figure 10-2 A, Axial computed tomography angiography (CTA) with right sigmoid sinus occlusion (black arrow) and dye present in the left sigmoid sinus (white arrow). B, Computed tomography (CT) venogram confirming the left internal jugular vein compressed between the styloid process (black arrow) and lateral mass of C1 (white arrow). C, Three-dimensional CTA demonstrating the left internal jugular vein compressed between the styloid process (black arrow) and lateral mass of C1 (white arrow). D, Left internal jugular vein, both compressed between the styloid and C1 lateral mass. E, Sagittal view of subsequent CTA demonstrating compression of the right internal jugular vein but some early recanalization.
(From Callahan B, Kang J, Dudekula A, et al: New Eagle’s syndrome variant complicating management of intracranial pressure after traumatic brain injury, Inj Extra 41:41-44, 2010.)

Clinically Relevant Anatomy
The styloid process extends in a caudal and ventral direction from the temporal bone from its origin just below the auditory meatus. The stylohyoid ligament’s cephalad attachment is to the styloid process, and its caudal attachment is to the hyoid bone. In Eagle syndrome the styloid process is abnormally elongated, either alone or in combination with calcification of the stylohyoid ligament. The elongated process or calcified ligament impinges on the internal carotid artery and branches of the glossopharyngeal nerve ( Figure 10-3 ). The glossopharyngeal nerve exits from the jugular foramen in proximity to the vagus and accessory nerves and the internal jugular vein and passes just inferior to the styloid process (see Figure 10-3 ). All three nerves lie in the groove between the internal jugular vein and the internal carotid artery.

Figure 10-3 In patients with Eagle syndrome, the abnormally elongated styloid process impinges on the internal carotid artery and glossopharyngeal nerve.
The key landmark for injection when treating Eagle syndrome is the styloid process of the temporal bone. This osseous process represents the calcification of the cephalad end of the stylohyoid ligament. Although the styloid process is usually easy to identify, if ossification is limited it may be difficult to locate with the exploring needle.

Technique
The patient is placed in the supine position. An imaginary line that runs from the mastoid process to the angle of the mandible ( Figure 10-4 ) is visualized. The styloid process should lie just below the midpoint of this line. The skin is prepared with antiseptic solution. A 22-gauge, 1½-inch needle attached to a 10-mL syringe is advanced at this midpoint location in a plane perpendicular to the skin. The styloid process should be encountered within 10 cm. After contact has been made, the needle is withdrawn slightly out of the periosteum or substance of the calcified ligament. After careful aspiration reveals no blood or cerebrospinal fluid, 5 mL of 0.5% preservative-free lidocaine combined with 80 mg of methylprednisolone is injected in incremental doses. Subsequent daily nerve blocks are carried out in a similar manner, substituting 40 mg of methylprednisolone for the initial 80-mg dose.

Figure 10-4 For proper needle placement when Eagle syndrome is treated, an imaginary line is drawn from the mastoid process to the angle of the mandible to facilitate locating the styloid process.

Side Effects and Complications
The major complications associated with this injection technique are related to trauma to the internal jugular vein and carotid artery. Hematoma formation and intravascular injection of local anesthetic with subsequent toxicity are not uncommon complications. Inadvertent blockade of the motor portion of the glossopharyngeal nerve can result in dysphagia secondary to weakness of the stylopharyngeus muscle. If the vagus nerve is inadvertently blocked, dysphonia secondary to paralysis of the ipsilateral vocal cord may occur. A reflex tachycardia secondary to vagal nerve block is also observed in some patients. Inadvertent block of the hypoglossal and spinal accessory nerves during glossopharyngeal nerve block will result in weakness of the tongue and trapezius muscle.

Clinical Pearls
This injection technique for Eagle syndrome is a simple technique that can produce dramatic relief for patients reporting the just-described types of pain. The proximity of the styloid process to major vasculature makes the presence of postblock hematoma and ecchymosis a distinct possibility. Although these complications are usually transitory, their dramatic appearance can be quite upsetting to the patient; therefore the patient should be warned of this possibility before the procedure. The vascularity of this region also increases the incidence of inadvertent intravascular injection. Even small amounts of local anesthetic injected into the carotid artery at this level will result in local anesthetic toxicity and seizures. Incremental administration while carefully monitoring the patient for signs of local anesthetic toxicity helps avoid this complication.
Glossopharyngeal neuralgia can be distinguished from Eagle syndrome in that the pain of glossopharyngeal neuralgia is characterized by paroxysms of shocklike pain as in trigeminal neuralgia, rather than the sharp, shooting pain on movement that is associated with Eagle syndrome. Because glossopharyngeal neuralgia may be associated with serious cardiac bradyarrhythmias and syncope, the clinician must distinguish between the two syndromes.
The clinician should always evaluate the patient with pain in this anatomic region for occult malignancy. Tumors of the larynx, hypopharynx, and anterior triangle of the neck may manifest as clinical symptoms identical to hyoid syndrome. Given the low incidence of Eagle syndrome relative to pain secondary to malignancy in this anatomic region, Eagle syndrome must be considered a diagnosis of exclusion.

Suggested Readings

Andrade M.G., Marchionni A.M., Rebello I.C., et al. Three-dimensional identification of vascular compression in Eagle’s syndrome using computed tomography: case report. J Oral Maxillofac Surg . 2008;66:169–176.
Callahan B., Kang J., Dudekula A., et al. New Eagle’s syndrome variant complicating management of intracranial pressure after traumatic brain injury. Inj Extra . 2010;41:41–44.
Lee S., Hillel A. Three-dimensional computed tomography imaging of eagle’s syndrome. Am J Otolaryngol . 2004;25:109.
Mendelsohn A.H., Berke G.S., Chhetri D.K. Heterogeneity in the clinical presentation of Eagle’s syndrome. Otolaryngol Head Neck Surg . 2006;134:389–393.
Olusesi A.D. More on heterogeneity of clinical presentation of Eagle’s syndrome. Otolaryngol Head Neck Surg . 2006;135:488.
Chapter 11 Stylohyoid Ligament Injection

Indications and Clinical Considerations
Hyoid syndrome is caused by calcification and inflammation of the attachment of the stylohyoid ligament to the hyoid bone. Tendinitis of the other muscular attachments to the hyoid bone also may contribute to this painful condition. Hyoid syndrome also may be seen in conjunction with Eagle syndrome or as a sequela of traumatic injuries of the hyoid ( Figure 11-1 ). The pain of hyoid syndrome is sharp and stabbing and occurs with movement of the mandible, turning of the neck, or swallowing. The pain starts below the angle of the mandible and radiates into the anterolateral neck. The pain of hyoid syndrome often is referred to the ipsilateral ear. Some patients also may report a foreign body sensation in the pharynx. Injection of the attachment of the stylohyoid ligament to the greater cornu of hyoid bone with local anesthetic and corticosteroid will serve as both a diagnostic and a therapeutic maneuver.

Figure 11-1 Bilateral hyoid bone fracture with disarticulation of the greater horns from the body, thyroid cartilage injury, mandibular symphyseal fracture, and left condyle fracture.
(From Badiali G, Pasquini E, Piccin O, Marchetti C: Injury risk related to the helmet strap: mandible and hyoid bone fractures with a hyoepiglottic ligament lesion, Inj Extra 41:89-91, 2010.)

Clinically Relevant Anatomy
The styloid process extends in a caudal and ventral direction from the temporal bone from its origin just below the auditory meatus. The stylohyoid ligament’s cephalad attachment is to the styloid process, and its caudal attachment is to the hyoid bone. In hyoid syndrome, the stylohyoid ligament becomes calcified at its caudal attachment to the hyoid bone ( Figure 11-2 ). Tendinitis of the other muscular attachments to the hyoid bone may also occur, contributing to the pain symptomatology.

Figure 11-2 Hyoid syndrome is usually caused by calcification of the stylohyoid ligament at its caudal attachment to the hyoid bone.
The key landmark for injection when treating hyoid syndrome is the cornu of the hyoid bone at a point between the mandible and the larynx. This osseous process is more easily identified if the greater cornu of the hyoid on the opposite side is steadied. Given the relationship of the great vessels of the neck to the greater cornu of the hyoid, care must be taken when placing needles in this anatomic area.

Technique
The patient is placed in the supine position. The angle of the mandible on the affected side is then identified. The greater cornu of the hyoid bone should lie approximately 1 inch inferior to the angle of the mandible. Gentle pressure at the same point on the contralateral side of the neck will steady the hyoid bone and make identification of the greater cornu and subsequent injection easier ( Figure 11-3 ). The skin is prepared with antiseptic solution. A 22-gauge, 1½-inch needle attached to a 10-mL syringe is advanced at the point 1 inch inferior to the angle of the mandible in a plane perpendicular to the skin. The greater cornu of the hyoid bone should be encountered within 2.5 to 3 cm (see Figure 11-2 ). After contact has been made, the needle is withdrawn slightly out of the periosteum or substance of the calcified ligament. After careful aspiration reveals no blood or cerebrospinal fluid, 5 mL of 0.5% preservative-free lidocaine combined with 80 mg of methylprednisolone is injected in incremental doses. Subsequent daily nerve blocks are carried out in a similar manner, substituting 110 mg of methylprednisolone for the initial 80-mg dose.

Figure 11-3 The hyoid bone can be stabilized by placing gentle pressure on the contralateral side of the hyoid bone, which will facilitate injection of the calcified ligamentous attachment.

Side Effects and Complications
This anatomic region is highly vascular, and because of the proximity of major vessels, the pain specialist should carefully observe the patient for signs of local anesthetic toxicity during injection. This vascularity and proximity to major blood vessels also give rise to an increased incidence of postblock ecchymosis and hematoma formation; the patient should be warned of such. In spite of the vascularity of this anatomic region, this technique can be safely performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also will decrease the amount of postprocedure pain and bleeding the patient may experience.
Because of the proximity to the spinal column, it also is possible to inadvertently inject the local anesthetic solution into the epidural, subdural, or subarachnoid space. At this level, even small amounts of local anesthetic placed into the subarachnoid space may result in total spinal anesthesia. If needle placement is too inferior, pneumothorax is possible because the dome of the lung lies at the level of the C7-T1 interspace.
Additional side effects associated with the injection of local anesthetic and corticosteroid in the treatment of hyoid syndrome include inadvertent block of the recurrent laryngeal nerve with associated hoarseness and dysphagia and the sensation that there is a lump in the throat when swallowing. Horner syndrome occurs when the superior cervical sympathetic ganglion is inadvertently blocked during this technique. The patient should be warned of the possibility of these complications before injection of local anesthetic and corticosteroid in the region of the greater cornua of the hyoid bone.

Clinical Pearls
This injection technique for hyoid syndrome is a simple one that can produce dramatic relief for patients experiencing the just-described types of pain. The proximity of the greater cornu of the hyoid bone to major vasculature makes postblock hematoma and ecchymosis a distinct possibility. Although these complications are usually transitory, their dramatic appearance can be quite upsetting to the patient; therefore the patient should be warned of such a possibility before the procedure. The vascularity of this region also increases the incidence of inadvertent intravascular injection. Even small amounts of local anesthetic injected into the carotid artery at this level will result in local anesthetic toxicity and seizures. Incremental administration while carefully monitoring the patient for signs of local anesthetic toxicity will help avoid this complication.
Glossopharyngeal neuralgia can be distinguished from hyoid syndrome in that the pain of glossopharyngeal neuralgia is characterized by paroxysms of shocklike pain as in trigeminal neuralgia, rather than the sharp, shooting pain that occurs on movement associated with hyoid syndrome. Because glossopharyngeal neuralgia may be associated with serious cardiac bradyarrhythmias and syncope, the clinician must distinguish the two syndromes.
The clinician should always evaluate the patient with pain in this anatomic region for occult malignancy. Tumors of the larynx, hypopharynx, and anterior triangle of the neck may cause clinical symptoms identical to those of hyoid syndrome. Given the low incidence of hyoid syndrome relative to pain secondary to malignancy in this anatomic region, hyoid syndrome must be considered a diagnosis of exclusion.

Suggested Readings

Badiali G., Pasquini E., Piccin O., Marchetti C. Injury risk related to the helmet strap: mandible and hyoid bone fractures with a hyoepiglottic ligament lesion. Inj Extra . 2010;41:89–91.
Ernest E.A., 3rd., Salter E.G. Hyoid bone syndrome: a degenerative injury of the middle pharyngeal constrictor muscle with photomicroscopic evidence of insertion tendinosis. J Prosthet Dent . 1991;66:78–83.
Nir D., Hefer T., Joachims H.Z. Hyoid bone syndrome and its treatment with nonsteroidal anti-inflammatory drugs. Am J Otolaryngol . 1998;19:296–300.
Rubin M.M., Sanfilippo R.J. Osteomyelitis of the hyoid caused by Torulopsis glabrata in a patient with acquired immunodeficiency syndrome. J Oral Maxillofac Surg . 1990;48:1217–1219.
Waldman S.D. Hyoid syndrome. Waldman S.D., ed. Atlas of uncommon pain syndromes, ed 2, Philadelphia: Saunders, 2008.
Chapter 12 Nasociliary Nerve Block

Indications and Clinical Considerations
Nasociliary nerve block is useful in the diagnosis and treatment of Charlin syndrome, which is also known as nasociliary neuralgia. Although as with most headache syndromes the exact cause of the pain of Charlin syndrome is unknown, the pathogenesis of this uncommon source of head and face pain is thought to be dysfunction of the nasociliary ganglion in a manner analogous to the dysfunction of the sphenopalatine ganglion that is thought to be the source of cluster headache. The presenting symptom of patients with Charlin syndrome is severe paroxysms of ocular or retro-orbital pain that radiates into the ipsilateral forehead, nose, and maxillary region. This pain is associated with voluminous ipsilateral rhinorrhea and congestion of the nasal mucosa as well as significant inflammation of the affected eye. The pain of Charlin syndrome has a rapid onset to peak, with attacks lasting 45 to 60 minutes. In some patients these attacks can be triggered by sensory stimulation of the affected areas. Although in many ways similar to cluster headache (e.g., the retro-orbital location of pain, profuse unilateral rhinorrhea, the rapid onset to peak, and the short duration of attacks), there are many dissimilarities. Unlike in cluster headache, alcohol does not seem to trigger attacks of Charlin syndrome, and the seasonal and chronobiologic patterns so characteristic of cluster headache appear to be absent ( Table 12-1 ). Furthermore, blockade of the sphenopalatine ganglion, which is so effective in the treatment of cluster headache, is of little value in the treatment of Charlin syndrome, whereas patients with Charlin syndrome uniformly respond to daily nasociliary nerve blocks with local anesthetic, as described later.
TABLE 12-1 Comparison of Cluster Headache and Charlin Syndrome   Cluster Headache Charlin Syndrome Ocular and retro-orbital location Yes Yes Unilateral Yes Yes Rapid onset to peak Yes Yes Severe intensity Yes Yes Attacks occur in paroxysms Yes Yes Duration of attacks is short Yes Yes Pain free between attacks Yes Yes Significant rhinorrhea during attacks Yes Yes Alcohol triggers attacks Yes No Tactile trigger areas No Yes Seasonal pattern of attacks Yes No Chronobiologic pattern of attacks Yes Yes Significant eye inflammation No Yes Responds to sphenopalatine ganglion block Yes No Responds to nasociliary block No Yes

Clinically Relevant Anatomy
The first division of the trigeminal nerve is the ophthalmic nerve, which provides sensory innervation to the cornea, iris, ciliary body, conjunctiva, and associated lacrimal gland. Branches of the ophthalmic nerve provide sensory innervation to the skin of the eyelid, forehead, and nose, as well as providing sensory innervation to portions of the nasal mucosa. The ophthalmic nerve arises from the superior portion of the gasserian ganglion and passes forward along the lateral wall of the cavernous sinus. Just before entering the orbit via the superior orbital fissure, the ophthalmic nerve divides into the lacrimal, frontal, and nasociliary branches ( Figure 12-1 ). The nasociliary branch enters the orbit between the two heads of the rectus lateralis muscle and between the superior or inferior rami of the oculomotor nerve. The nasociliary nerve then passes across the ipsilateral optic nerve to the medial wall of the orbital cavity to pass through the anterior ethmoidal foramen to cross the lateral margin of the cribriform plate of the ethmoid bone into the nasal cavity, where the internal nasal branch provides sensory innervation to the anterior nasal septum and lateral wall of the nasal cavity. The external nasal branch of the nasociliary nerve provides sensory innervation to the skin of the ala and apex of the nose.

Figure 12-1 Just before entering the orbit, the ophthalmic nerve divides into the lacrimal, frontal, and nasociliary branches.
In addition to the internal and external nasal branches, the nasociliary nerves give off branches including the long ciliary branch; the long root of the ciliary ganglion branch is intimately involved with sympathetic fibers from the deep cervical plexus and ciliary ganglion. Some investigators believe that there are also small intercommunications between these branches and the sphenopalatine ganglion.

Technique
The patient is placed in a supine position. A total of 2 mL of local anesthetic is drawn up in a 10-mL sterile syringe. When treating Charlin syndrome with nasociliary nerve block via the medial orbital approach, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks.
To perform blockade of the nasociliary nerve, the medial canthus is identified and a line is drawn superiorly to a point just below the eyebrow ( Figure 12-2 ). The skin overlying this area is prepared with antiseptic solution, with care being taken to avoid spillage into the eye. A 22-gauge, 1½-inch needle is inserted at this point, and, with close contact kept with the bony surface of the orbit, the needle is carefully advanced posteroinferiorly approximately 35 degrees off the perpendicular to a depth of approximately 1¼ inches ( Figure 12-3 ). After careful gentle aspiration, the contents of the syringe are slowly injected. Because of the loose alveolar tissue of the eyelid, a gauze sponge should be used to apply gentle pressure on the upper eyelid and supraorbital tissues before injection of solution to prevent the injectate from dissecting inferiorly into these tissues. This pressure should be maintained after the procedure to avoid periorbital hematoma and ecchymosis. When nasociliary nerve block is used to treat the pain and symptoms associated with Charlin syndrome, 8 to 10 daily nerve blocks with local anesthetic may be required. If daily blocks are being performed, as a general rule the total dose of depot corticosteroids included in these blocks should not exceed 360 to 400 mg.

Figure 12-2 For identification of the nasociliary nerve, an imaginary line is drawn from the medial canthus to a point just below the eyebrow.

Figure 12-3 When a nasociliary nerve block is performed, the needle tip is advanced while close contact is maintained with the bony surface of the orbit to avoid trauma to the globe.

Side Effects and Complications
The major complication of this procedure is inadvertent injury to the eye. Failure to maintain bony contact while the needle is advanced will greatly increase the risk of the devastating complication. The practitioner should also remember that this area is highly vascular, and the potential for intravascular injection of local anesthetic with its attendant risks remains an ever-present possibility. This vascularity gives rise to an increased incidence of postblock ecchymosis and hematoma formation. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding.

Clinical Pearls
Nasociliary nerve block via the medial orbital approach is especially useful in the diagnosis and palliation of pain secondary to Charlin syndrome. Given the uncommon nature of this headache syndrome and its overlap with the symptoms of cluster headache as well as other neurologic problems, including multiple sclerosis, cavernous sinus thrombosis, and intracranial and retro-orbital tumors, Charlin syndrome must remain a diagnosis of exclusion ( Figure 12-4 ). All patients suspected of having Charlin syndrome require magnetic resonance imaging (MRI) of the brain with and without gadolinium contrast as well as thorough ophthalmologic and neurologic evaluation. Nasociliary nerve block via the medial orbital approach should be performed only by those familiar with the regional anatomy.

Figure 12-4 A 20-year-old man with known multiple sclerosis and hypoesthesia and pain in the distribution of the left trigeminal nerve. A, T2-weighted axial image shows an area of increased signal intensity (arrow) involving the left lateral pons and extending into the root entry zone of the left trigeminal nerve. B, Unenhanced T1-weighted image shows that the hypointense lesion is well defined (arrow). C, Contrast-enhanced T1-weighted image shows no enhancement (arrow), suggesting an inactive plaque.
(From Becker M, Kohler R, Vargas MI, et al: Pathology of the trigeminal nerve, Neuroimaging Clin N Am 18:283-307, 2008.)

Suggested Readings

Baker B.L., Fosko S.W. The nose: principles of surgical treatment. Adv Dermatol . 2008;24:112–132.
Becker M., Kohler R., Vargas M.I., et al. Pathology of the trigeminal nerve. Neuroimaging Clin N Am . 2008;18:283–307.
Huibin Q., Jianxing L., Guangyu H., Dianen F. The treatment of first division idiopathic trigeminal neuralgia with radiofrequency thermocoagulation of the peripheral branches compared to conventional radiofrequency. J Clin Neurosci . 16, 2009. 14212–1429
Rait J. Ocular causes of headache. In: Selvaratnam P., Niere K., Zuluaga M. Headache, orofacial pain and bruxism . New York: Churchill Livingstone; 2009:127–138.
Rozen T. Post-traumatic external nasal pain syndrome (a trigeminal based pain disorder). Headache . 2009;49:1223–1228.
Chapter 13 Auriculotemporal Nerve Block

Indications and Clinical Considerations
Frey syndrome is a constellation of symptoms including unilateral hyperhidrosis and flushing of the malar region and pinna of the ear that occurs when eating or drinking anything that stimulates the parotid gland to produce saliva ( Figure 13-1 ). Also known as auriculotemporal syndrome, Baillarger syndrome, Dupuy syndrome, salivosudoriparous syndrome, and gustatory sweating syndrome, this disorder usually occurs 2 to 13 months after surgery, open trauma, or infection of the parotid gland. It is thought to be caused by improper regeneration of the sympathetic and parasympathetic nerves subserving the parotid gland and affected anatomic areas. The severity of symptoms associated with Frey syndrome can range from mild to debilitating. Although the incidence of Frey syndrome after parotid surgery can be decreased by careful attention to surgical technique, including careful identification and preservation of auriculotemporal nerve and creation of a thick skin flap when performing parotidectomy, approximately 5% of patients undergoing parotid surgery will experience some degree of symptomatology. For patients with mild symptoms, reassurance and the use of topical antiperspirants such as 20% aluminum chloride in alcohol or topical scopolamine cream may be all that is required. For more severe symptoms, blockade of the auriculotemporal nerve may provide significant relief. Auriculotemporal nerve block may also be combined with intradermal injection of botulinum toxin A in the areas of hyperhidrosis.

Figure 13-1 Patients with Frey syndrome experience unilateral hyperhidrosis and flushing of the malar region.

Clinically Relevant Anatomy
The auriculotemporal nerve arises from fibers of the mandibular nerve. The auriculotemporal nerve courses upward through the parotid gland, passing between the temporomandibular joint and the external auditory meatus, where it gives off branches that provide sensory innervation to the temporomandibular joint and portions of the pinna of the ear and the external auditory meatus. Ascending over the origin of the zygomatic arch, the auriculotemporal nerve continues upward along with the temporal artery, providing sensory innervation to the temporal region and lateral scalp.

Technique
The patient is placed in the supine position with the head turned away from the side to be blocked. A total of 5 mL of local anesthetic is drawn up in a 12-mL sterile syringe. When painful conditions involving the auriculotemporal nerve that may have an inflammatory component are treated, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks.
The temporal artery is identified at a point just above the origin of the zygoma on the affected side. After preparation of the skin with antiseptic solution, a 25-gauge, 1½-inch needle is inserted at this point and is advanced perpendicularly until the needle approaches the periosteum of the underlying bone ( Figure 13-2 ). A paresthesia may be elicited, and the patient should be warned of this possibility. After gentle aspiration, 3 mL of solution is injected. The needle is then redirected in a cephalad trajectory; after careful aspiration, the remaining 2 mL of solution is injected in a fanlike manner.

Figure 13-2 The auriculotemporal nerve arises from fibers of the mandibular nerve and is blocked at the point just above the origin of the zygoma.

Side Effects and Complications
The scalp is highly vascular, and the auriculotemporal nerve is in proximity to the temporal artery at the point at which the nerve is blocked. Therefore the pain specialist should carefully calculate the total milligram dose of local anesthetic that may be safely given, especially if bilateral nerve blocks are being performed. This vascularity gives rise to an increased incidence of postblock ecchymosis and hematoma formation. Despite the vascularity of this anatomic region, this technique can be safely performed in the presence of anticoagulation by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.

Clinical Pearls
Auriculotemporal block is a useful technique in the management of the symptoms of Frey syndrome that fail conservative therapy, including reassurance and topical antiperspirants. The exact mechanism of how auriculotemporal nerve block relieves the symptoms of Frey syndrome is unknown, but it is plausible to ascribe a neuroanatomic basis for this technique’s efficacy given the interrelation of the auriculotemporal nerve with the abundant sympathetic and parasympathetic fibers that may serve as the nidus of this unusual syndrome. The concomitant use of interdermal injections of botulinum toxin A may further improve symptom relief if auriculotemporal nerve block alone fails to provide satisfactory results.

Suggested Readings

Cantarella G., Berlusconi A., Mele V., et al. Treatment of Frey’s syndrome with botulinum toxin type B. Otolaryngol Head Neck Surg . 2010;143:214–218.
Hoff S.R., Mohyuddin N., Yao M. Complications of parotid surgery. Oper Tech Otolaryngol Head Neck Surg . 2009;20:123–130.
Moreno-Arias G.A., Grimalt R., Llusa M., et al. Frey’s syndrome. J Pediatr . 2001;138:294.
O’Neill J.P., Condron C., Curran A., Walsh M. Lucja Frey—historical relevance and syndrome review. Surgeon . 2008;6:178–181.
Rustemeyer J., Eufinger H., Bremerich A. The incidence of Frey’s syndrome. J Craniomaxillofac Surg . 2008;36:34–37.
Chapter 14 Omohyoid Muscle Injection

Indications and Clinical Considerations
Omohyoid syndrome is caused by trauma to the fibers of the inferior belly of the omohyoid muscle. The syndrome is seen most often in patients who have recently experienced a bout of intense vomiting or sustained a flexion-extension injury to the cervical spine and to the musculature of the anterior neck. Concurrent trauma to the brachial plexus with upper extremity symptomatology also may accompany trauma-induced omohyoid syndrome. The pain of omohyoid syndrome manifests as myofascial pain. It is constant and exacerbated with movement of the affected muscle. A trigger point in the inferior belly of the omohyoid muscle is often present and provides a basis for treatment. The pain of omohyoid syndrome starts just above the clavicle at the lateral aspect of the clavicular attachment of the sternocleidomastoid muscle. The pain may radiate into the anterolateral neck. Injection of the trigger point in the inferior muscle of the omohyoid muscle with local anesthetic and corticosteroid serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy
The omohyoid muscle extends from the hyoid bone laterally and inferiorly to the insertion at the upper margin of the scapula ( Figure 14-1 ). The intermediate tendon of the omohyoid muscle that runs from the muscle inferiorly to attach at the clavicle tethers the muscle down, and the point of musculotendinous insertion is susceptible to trauma. The inferior portion of the omohyoid muscle is further confined by the overlying attachment of the sternocleidomastoid to the clavicle. The omohyoid muscle also is susceptible to trauma at this point. The internal jugular vein and common carotid artery lie deep to the omohyoid muscle. The brachial plexus lies more lateral.

Figure 14-1 The omohyoid muscle extends from the hyoid bone laterally and inferiorly to its insertion at the upper margin of the scapula.
The key landmark for injection when treating omohyoid syndrome is the lateral aspect of the clavicular head of the sternocleidomastoid muscle (see Figure 14-1 ). The omohyoid muscle is located slightly lateral and deep to the clavicular head of the sternocleidomastoid muscle, ½ to 1 inch above the superior margin of the clavicle. Given the relationship of the great vessels of the neck to the omohyoid muscle, care must be taken when placing needles in this anatomic area.

Technique
The patient is placed in a supine position with the head turned away from the side to be blocked. A total of 3.0 mL of local anesthetic is drawn up in a 5.0-mL sterile syringe. When omohyoid syndrome is treated, a total of 80 mg of depot corticosteroid is added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks.
The patient is then asked to raise his or her head against the resistance of the pain specialist’s hand to aid in identification of the posterior border of the sternocleidomastoid muscle. The point at which the lateral border of the sternocleidomastoid attaches to the clavicle is then identified. At this point, slightly lateral and approximately 1 inch above the clavicle, after preparation of the skin with antiseptic solution, a 1½-inch needle is inserted directly perpendicular to the tabletop (see Figure 14-1 ). The needle should be advanced quite slowly because of proximity of the great vessels and brachial plexus. A pop is often felt as the fascia of the omohyoid muscle is pierced. This should occur at a depth of ½ to 3 4 inch. If strict attention to technique is observed and the needle has not been placed or directed too laterally, the brachial plexus should not be encountered. However, because of the proximity of the brachial plexus, the patient should be warned that a paresthesia could occur and to say “there!” should a paresthesia be felt. The needle should never be directed in a more inferomedial trajectory, or pneumothorax is likely to occur.
After the muscle has been identified, gentle aspiration is carried out to identify blood or cerebrospinal fluid. If the aspiration test result is negative and no paresthesia into the distribution of the brachial plexus is encountered, 3.0 mL of solution is slowly injected, with the patient being monitored closely for signs of local anesthetic toxicity or inadvertent neuraxial injection.

Side Effects and Complications
The proximity to the great vessels of the neck suggests the potential for inadvertent intravascular injection or local anesthetic toxicity from intravascular absorption. This vascularity also gives rise to an increased incidence of postblock ecchymosis and hematoma formation. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. Application of cold packs for 20-minute periods after the block will also decrease the amount of postprocedure pain and bleeding the patient may experience.
In addition to the potential for complications involving the vasculature, should the needle be placed too laterally, the proximity of the brachial plexus, the central neuraxial structures, and the phrenic nerve can result in side effects and complications. Although these complications should be rare if proper technique is observed, the potential for inadvertent epidural, subdural, or subarachnoid injection remains. If the local anesthetic used for this block is accidentally placed in any of these spaces, significant motor and sensory block may result. If unrecognized, these complications could be fatal. Phrenic nerve block also can occur when this injection technique is used to treat omohyoid syndrome if the needle placement is too posterolateral. In the absence of significant pulmonary disease, unilateral phrenic nerve block rarely should create respiratory embarrassment. However, blockade of the recurrent laryngeal nerve with its attendant vocal cord paralysis, combined with paralysis of the diaphragm, may make the clearing of pulmonary and upper airway secretions difficult. Because of the proximity of the apex of the lung, pneumothorax is a distinct possibility and the patient should be informed of this.

Clinical Pearls
The key to safely performing this injection technique is a clear understanding of the anatomy and careful identification of the anatomic landmarks necessary to perform the block. The clinician should remember that the brachial plexus is quite superficial at the level at which this block is performed. The needle should rarely be inserted deeper than ¾ inch in all but the most obese patients. If strict adherence to technique is observed and the needle is never advanced medially from the lateral border of the insertion of the sternocleidomastoid muscle on the clavicle, the incidence of pneumothorax should be less than 0.5%.
In the absence of well-documented trauma to the anterior neck, omohyoid syndrome is a diagnosis of exclusion. The clinician should always evaluate the patient with pain in this anatomic region for occult malignancy. Tumors of the larynx, hypopharynx, and anterior triangle of the neck may cause clinical symptoms identical to omohyoid syndrome. In the setting of flexion-extension injuries or other forceful trauma to the soft tissues of the neck or cervical spine, the clinician also should evaluate the patient for trauma to the brachial plexus by careful physical examination and the use of electromyography.

Suggested Readings

Kim L., Kwon H., Pyun S.B. Pseudodysphagia due to omohyoid muscle syndrome. Dysphagia . 2009;24:357–361.
Waldman S.D. Omohyoid syndrome. Waldman S.D., ed. Atlas of uncommon pain syndromes, ed 2, Philadelphia: Saunders, 2008.
Wong D.S., Li J.H. The omohyoid sling syndrome. Am J Otolaryngol . 2000;21:318–322.
Zachary R.B., Young A., Hammond J.D. The omohyoid syndrome. Lancet . 1969;294:104–105.
Chapter 15 Trigeminal Nerve Block

Indications and Clinical Considerations
Trigeminal neuralgia is an episodic pain that affects the areas of the face supplied by the trigeminal nerve. The pain is unilateral in 97% of cases reported. When it does occur bilaterally, it is in the same division of the nerve. The second or third division of the nerve is affected in the majority of patients, with the first division affected less than 5% of the time. The pain develops on the right side of the face in unilateral disease 57% of the time. The pain is characterized by paroxysms of electric shock–like pain lasting from several seconds to less than 2 minutes. The progression from onset to peak is essentially instantaneous.
The patient with trigeminal neuralgia will go to great lengths to avoid any contact with trigger areas. Persons with other types of facial pain, such as temporomandibular joint dysfunction, tend to constantly rub the affected area or apply heat or cold to it. Patients with uncontrolled trigeminal neuralgia frequently require hospitalization for rapid control of pain. Between attacks, the patient is relatively pain free. A dull ache remaining after the intense pain subsides may indicate a persistent compression of the nerve by a structural lesion. This disease is almost never seen in people younger than 30 unless it is associated with multiple sclerosis.
The patient with trigeminal neuralgia will often have severe and at times even suicidal depression with high levels of superimposed anxiety during acute attacks. Both of these problems may by exacerbated by the sleep deprivation that often occurs during episodes of pain. Patients with coexisting multiple sclerosis may exhibit the euphoric dementia characteristic of that disease.
The mainstay of the treatment of trigeminal neuralgia is pharmacologic, with carbamazepine and baclofen being drugs of first choice. Other anticonvulsants, including pregabalin, gabapentin, and oxcarbazepine, may also be beneficial. For patients whose condition fails to respond to pharmacologic treatment, trigeminal nerve block via the coronoid approach may be a next reasonable step. If conservative treatment fails, more invasive options including radiofrequency lesioning, balloon compression, Gamma Knife radiosurgery, and microvascular decompression may be considered with a careful assessment of the risk-to-benefit ratio for each procedure.

Clinically Relevant Anatomy
The maxillary division (V2) of the trigeminal nerve is a pure sensory nerve ( Figure 15-1 ). It exits the middle cranial fossa via the foramen rotundum and crosses the pterygopalatine fossa ( Figure 15-2 ). Passing through the inferior orbital fissure, it enters the orbit, emerging on the face via the infraorbital foramen. The maxillary nerve can be selectively blocked by placing a needle just above the anterior margin of the lateral pterygoid plate.

Figure 15-1 The trigeminal nerve is divided into three divisions.
(From Waldman SD: Atlas of Interventional Pain Management, ed 2, Philadelphia, 2003, Saunders.)

Figure 15-2 T1-weighted image through left face medial to the mandible, demonstrating the maxillary sinus (M), orbital surface of the maxilla (open white arrow), medial aspect of the pterygopalatine fossa (white arrowhead), retroantral fat pad (solid white arrow), lateral pterygoid muscle fibers coursing to the proximal mandible (L), marrow in the maxilla (solid white arrow 1) and mandible (solid white arrow 2), sublingual space (small black arrow), geniohyoid muscle (G), and hyoid bone (large black arrow).
(From Stark DD, Bradley WG Jr: Magnetic resonance imaging, ed 3, St Louis, 1999, Mosby.)
The maxillary nerve provides sensory innervation for the dura of the middle cranial fossa, the temporal and lateral zygomatic region, and the mucosa of the maxillary sinus. The nerve also provides sensory innervation for the upper molars, premolars, incisors, canines, and associated oral gingiva as well as the mucous membranes of the cheek. The nasal cavity, lower eyelid, skin of the side of the nose, and the upper lip are also subserved by the maxillary nerve.
The mandibular division (V3) is composed of a large sensory root and smaller motor root. Both leave the middle cranial fossa together via the foramen ovale and join to form the mandibular nerve. Branches of the mandibular nerve provide sensory innervation to portions of the dura mater and the mucosal lining of the mastoid sinus. Sensory innervation to the skin overlying the muscles of mastication, the tragus and helix of the ear, the posterior temporomandibular joint, the chin, and the dorsal aspect of the anterior two thirds of the tongue and associated mucosa of the oral cavity is also provided by the mandibular nerve (see Figure 15-1 ). The smaller motor branch provides innervation to the masseter, external pterygoid, and temporalis muscles.

Technique
The patient is placed in the supine position with the cervical spine in the neutral position. The coronoid notch is identified by asking the patient to open and close the mouth several times and palpating the area just anterior and slightly inferior to the acoustic auditory meatus. After the notch has been identified, the patient is asked to hold his or her mouth in neutral position.
A total of 7 mL of local anesthetic is drawn up in a 12-mL sterile syringe. When trigeminal neuralgia, atypical facial pain, or other painful conditions involving the maxillary and mandibular nerve are treated, a total of 150 mg of depot corticosteroid are added to the local anesthetic with the first block, and 40 mg of depot corticosteroid is added with subsequent blocks.
After the skin overlying the coronoid notch has been prepared with antiseptic solution, a 22-gauge, 3½-inch styletted needle is inserted just below the zygomatic arch directly in the middle of the coronoid notch. The needle is advanced 1½ to 2 inches in a plane perpendicular to the skull until the lateral pterygoid plate is encountered ( Figure 15-3 ). At this point, if blockade of both the maxillary and mandibular nerves is desired, the needle is withdrawn slightly. After careful aspiration, 7 to 15 mL of solution is injected in incremental doses. During the injection procedure the patient must be observed carefully for signs of local anesthetic toxicity.

Figure 15-3 For trigeminal nerve block to be performed, the needle is inserted in the middle of the coronoid notch and advanced toward the lateral pterygoid plate.
(From Waldman SD: Atlas of Interventional Pain Management , ed 2, Philadelphia, 2003, Saunders.)

Side Effects and Complications
Because of the highly vascular nature of the pterygopalatine fossa, significant facial hematoma may occur after trigeminal nerve block via the coronoid approach. This vascularity means that the pain specialist should use small, incremental doses of local anesthetic to avoid local anesthetic toxicity.
Postprocedure dysesthesia, including anesthesia dolorosa, may occur in a small number of patients who undergo neurodestructive procedures of the branches of the trigeminal nerve in an effort to palliate the pain of trigeminal neuralgia. These dysesthesias can range from mild pulling or burning sensations to severe postprocedure pain called anesthesia dolorosa. These postprocedure symptoms are thought to be caused by incomplete destruction of the neural structures. Sloughing of skin in the area of anesthesia may also occur.
In addition to disturbances of sensation, blockade or destruction of the branches of the trigeminal nerve may result in abnormal motor function, including weakness of the muscles of mastication and secondary facial asymmetry caused by muscle weakness or loss of proprioception. The patient should be warned that all of these complications may occur.

Clinical Pearls
Trigeminal nerve block via the coronoid approach with local anesthetic and corticosteroid represents an excellent option for patients with uncontrolled pain from trigeminal neuralgia that has not responded to pharmacologic management or for palliation of the acute pain of trigeminal neuralgia while waiting for drugs to take effect. The major side effects of this block are related to the vascular nature of the pterygopalatine fossa, and care must be taken to avoid local anesthetic toxicity. In spite of this vascularity, if a 25- or 27-gauge needle is used, this technique can safely be performed in the presence of anticoagulation, albeit at increased risk of facial hematoma, should the clinical situation dictate a favorable risk-to-benefit ratio.
Because repeated needle punctures of daily or every-other-day blocks may result in small punctate facial scars, patients should be warned of this possibility. Infection, although rare, remains an ever-present possibility, especially in immunocompromised patients. Early detection of infection is crucial to avoid potentially life-threatening sequelae.

Suggested Readings

Borges A., Casselman J. Imaging the trigeminal nerve. Eur J Radiol . 2010;74:323–340.
Dubey A., Sung W.S., Shaya M., et al. Complications of posterior cranial fossa surgery—an institutional experience of 500 patients. Surg Neurol . 2009;72:369–375.
Martin T., Mark R., Smith H., et al. Gamma Knife radiosurgery (GKRS) in the management of trigeminal neuralgia: long-term follow-up report of 511 cases. Int J Radiat Oncol Biol Phys . 2009;75(3 Suppl 1):S128–S129.
Waldman S.D. The trigeminal nerve—cranial nerve V. In: Pain review . Philadelphia: Saunders; 2009:15–16.
Waldman S.D. Trigeminal neuralgia. In Atlas of common pain syndromes , ed 2, Philadelphia: Saunders; 2008:29–32.
Waldman S.D. Trigeminal neuralgia. In: Pain review . Philadelphia: Saunders; 2009:220–222.
Chapter 16 Injection Technique for Trapezius Syndrome

Indications and Clinical Considerations
The muscles of the posterior neck are particularly susceptible to the development of myofascial pain syndrome. Flexion-extension injuries to the neck or repeated microtrauma secondary to pressure from the straps of purses, backpacks, or laptop computer cases may result in the development of myofascial pain in the trapezius.
Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain maybe misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the trapezius frequently have referred pain into the neck, mastoid region, angle of the jaw, and upper extremity—the last leading the patient to believe he or she is having a heart attack.
The trigger point is the pathognomonic lesion of myofascial pain and is thought to be the result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, often there is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This sign is also characteristic of myofascial pain syndrome.
Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are a result of microtrauma to the affected muscle. This microtrauma may occur as the result of a single injury to the affected muscle or as the result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit.
In addition to muscle trauma, a variety of other factors seem to predispose the patient to the development of myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. Poor posture while sitting at a computer keyboard or while watching television also has been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The trapezius muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome.
Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities including depression frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy
The muscles of the neck work together as a functional unit to stabilize and allow coordinated movement of the head and associated sense organs. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The trapezius is a primary extensor of the neck as well as part of the group of muscles known as the axioscapular group, which is involved in stabilization and movement of the scapula ( Figure 16-1 ). The upper trapezius originates at the ligamentum nuchae and the spinous processes of the cervical and upper thoracic spine and attaches to the upper margin of the scapula. The middle portion of the trapezius originates from the spinous processes of the upper thoracic spine and attaches to the medial border of the scapula. The lower fibers of the trapezius originate from the spinous processes of the lower thoracic spine and attach to the medial portion of the scapular spine. These points of origin of the trapezius and attachments are particularly susceptible to trauma and the subsequent development of myofascial trigger points (see Figure 16-1 ). Injection of these trigger points serves as both a diagnostic and a therapeutic maneuver.

Figure 16-1 The trapezius muscle is a primary extensor of the neck and is subject to the development of myofascial trigger points.

Technique
Careful preparation of the patient before trigger point injection helps optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality will be required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points as well as when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection.
After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle is adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications
The proximity to the spinal cord and exiting nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. The proximity to the vertebral artery combined with the vascular nature of this anatomic region makes the potential for intravascular injection high. Even small amounts of injection of local anesthetic into the vertebral arteries will result in seizures. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also report a transient increase in pain after injection of trigger points in the trapezius. If long needles are used, pneumothorax also may occur.

Clinical Pearls
Trigger point injections are an extremely safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space.
The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline represent good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin may also be of value in the pharmacologic management of myofascial pain syndromes.

Suggested Readings

Baldry P. Acupuncture treatment of fibromyalgia and myofascial pain. In: Chaitow L., ed. Fibromyalgia syndrome . ed 3. Oxford: Churchill Livingstone; 2010:145–159.
Ge H.Y., Nie H., Madeleine P., et al. Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome. Pain . 2009;147:233–240.
Ge H.Y., Wang Y., Danneskiold-Samsøe B., et al. The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points. J Pain . 2010;11:644–651.
LeBlanc K.E., LeBlanc L.L. Musculoskeletal disorders. Prim Care . 2010;37:389–406.
Lucas K.R., Rich P.A., Polus B.I. Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger points, Clin Biomech (Bristol. Avon) . 2010;25:765–770.
Partanen J.V., Ojala T.A., Arokoski J.P. Myofascial syndrome and pain: a neurophysiological approach. Pathophysiology . 2010;17:19–28.
Chapter 17 Injection Technique for Cervical Strain

Indications and Clinical Considerations
The muscles of the posterior neck are particularly susceptible to the development of acute and chronic pain symptomatology after acute flexion, extension, or lateral bending injuries to the neck or repeated microtrauma secondary to pressure from the straps of purses, backpacks, or laptop computer cases. These muscles also are adversely affected by chronic stress, a behavioral abnormality that may manifest itself clinically as cervical strain. Myofascial pain syndrome with its pathognomonic myofascial trigger points also may occur, either alone or in combination with cervical strain.
Cervical strain is the result of microtrauma or macrotrauma to the muscle fibers or the musculotendinous unit of the trapezius and the deep muscles of the posterior neck, including the splenius capitis and splenius cervicis. Clinically, cervical strain manifests as aching, tightness, stiffness, and pain in the neck and upper back, with pain radiating into the ipsilateral shoulder. As mentioned previously, cervical strain may coexist with myofascial pain syndrome, and trigger points also may be present. Symptoms of cervical strain can be reproduced with ipsilateral rotation and contralateral bending of the cervical spine. Tenderness to deep palpation is present, but unless myofascial pain syndrome is also present, trigger points should be absent. The pain, spasm, and other associated symptoms of cervical strain are aggravated with physical or emotional stress.

Clinically Relevant Anatomy
The muscles of the neck work together as a functional unit to stabilize and allow coordinated movement of the head and associated sense organs. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The trapezius, splenius capitis, splenius cervicis, and semispinalis capitis are the primary extensors of the neck, as well as part of the group of muscles known as the axioscapular group, which is involved in stabilization and movement of the scapula ( Figure 17-1 ). The upper trapezius originates at the ligamentum nuchae and the spinous processes of the cervical and upper thoracic spine and attaches to the upper margin of the scapula. The middle portion of the trapezius originates from the spinous processes of the upper thoracic spine and attaches to the medial border of the scapula. The lower fibers of the trapezius originate from the spinous processes of the lower thoracic spine and attach to the medial portion of the scapular spine. The splenius capitis arises from the lower part of the ligamentum nuchae and the upper four thoracic spinous processes and inserts into the superior nuchal line of the occipital bone. The splenius cervicis has a similar origin but inserts into the upper transverse process of the upper cervical vertebrae. These points of origin and attachments of these muscles are particularly susceptible to trauma and the subsequent development of strain or myofascial trigger points (see Figure 17-1 ). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Figure 17-1 The primary extensor muscles of the neck are susceptible to the development of acute and chronic pain syndromes.

Technique
The goals of this injection technique are explained to the patient, and proper preparation with antiseptic solution of the skin overlying the affected muscles is carried out. A syringe containing 17 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the affected muscle. The needle is then inserted into the body of the muscle (see Figure 17-1 ). A “pop” will usually be felt when the needle pierces the fascia. After careful aspiration, a volume of 5 to 7 mL is then gently injected in a fanlike fashion throughout the affected muscle. If myofascial trigger points are also present, a volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the symptoms of cervical strain and coexisting trigger points; the patient should be informed of this.

Side Effects and Complications
The proximity to the spinal cord and exiting nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. The proximity to the vertebral artery combined with the vascular nature of this anatomic region makes the potential for intravascular injection high. Even small amounts of injection of local anesthetic into the vertebral arteries will result in seizures. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after this injection technique is not an uncommon occurrence. Many patients also report a transient increase in pain after injection of the just-mentioned muscles. If long needles are used, pneumothorax may also occur.

Clinical Pearls
This injection technique is extremely effective in the treatment of cervical strain. Trigger point injections should be added if there is coexistent myofascial pain. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of the injection technique for cervical strain are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after this injection technique. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting muscles or myofascial trigger points in proximity to the underlying pleural space.
The use of physical modalities, including local heat and gentle stretching exercises, should be introduced several days after the patient has undergone this injection technique for cervical strain. Vigorous exercise should be avoided because it will exacerbate the patient’s symptomatology. Simple analgesics, nonsteroidal antiinflammatory agents, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique.
If myofascial pain coexists with the symptoms of cervical strain, tricyclic antidepressants should be considered. The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given in a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow.

Suggested Readings

Chen H.B., Yang K.H., Wang Z.G. Biomechanics of whiplash injury. Chin J Traumatol . 2009;12:305–314.
Cho C.H., Song K.S., Min B.W., et al. Musculoskeletal injuries in break-dancers. Injury . 2009;40:1207–1211.
Opper S.E. Neck pain. In: Smith H.S., ed. Current therapy in pain . Philadelphia: Saunders; 2009:137–147.
White K., Hudgins T.H., Alleva J.T. Cervical sprain/strain definition. Dis Mon . 2009;55:724–728.
Zmurko M.G., Tannoury T.Y., Tannoury C.A., Anderson D.G. Cervical sprains, disc herniations, minor fractures, and other cervical injuries in the athlete. Clin Sports Med . 2003;22:513–521.
Chapter 18 Injection Technique for Sternocleidomastoid Syndrome

Indications and Clinical Considerations
The sternocleidomastoid is particularly susceptible to the development of myofascial pain syndrome. Flexion-extension and lateral motion stretch injuries to the neck or repeated microtrauma secondary to jobs that require working overhead for long periods such as painting ceilings, reading in bed, or watching television while reclining on a couch may result in the development of myofascial pain in the sternocleidomastoid muscle.
Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the sternocleidomastoid often have referred pain into the upper neck, face, angle of the mandible, and temporal region.
The trigger point is the pathognomonic lesion of myofascial pain and is thought to be the result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to this local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome.
Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are the result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or may occur as the result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit.
In addition to muscle trauma, various other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The sternocleidomastoid muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome.
Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy
The muscles of the neck work together as a functional unit to stabilize and allow coordinated movement of the head and associated sense organs. Trauma to an individual muscle can result in dysfunction of the entire functional unit. The sternocleidomastoid extends the head at the atlantooccipital joint and rotates the head to the contralateral side. The origin of the sternocleidomastoid is by a muscular head from the medial third of the clavicle and a rounded tendon from the front of the sternal manubrium ( Figure 18-1 ). The muscle inserts into the mastoid process of the temporal bone and the occipital bone. These points of origin of the sternocleidomastoid and attachments are particularly susceptible to trauma and the subsequent development of myofascial trigger points (see Figure 18-1 ). Injection of these trigger points serves as both a diagnostic and a therapeutic maneuver.

Figure 18-1 Patients with sternocleidomastoid pain syndrome often experience referred pain to the upper neck, face, angle of the mandible, and temporal region.

Technique
Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important that the patient understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection.
After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications
The proximity to the spinal cord and exiting nerve roots, as well as the great vessels of the neck, makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. The proximity to the carotid artery and jugular vein, combined with the vascular nature of this anatomic region, makes the potential for intravascular injection high. Even small amounts of injection of local anesthetic into the carotid artery will result in seizures. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also complain of a transient increase in pain after injection of trigger points in the sternocleidomastoid. If long needles are used, pneumothorax may also occur.

Clinical Pearls
Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space.
The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline are good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin may also be of value in the pharmacologic management of myofascial pain syndromes.

Suggested Readings

Baldry P. Acupuncture treatment of fibromyalgia and myofascial pain. In: Chaitow L., ed. Fibromyalgia syndrome . ed 3. Oxford: Churchill Livingstone; 2010:145–159.
Ge H.Y., Nie H., Madeleine P., et al. Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome. Pain . 2009;147:233–240.
Ge H.Y., Wang Y., Danneskiold-Samsøe B., et al. The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points. J Pain . 2010;11:644–651.
LeBlanc K.E., LeBlanc L.L. Musculoskeletal disorders. Prim Care . 2010;37:389–406.
Lucas K.R., Rich P.A., Polus B.I. Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger points. Clin Biomech (Bristol, Avon) . 2010;25:765–770.
Partanen J.V., Ojala T.A., Arokoski J.P. Myofascial syndrome and pain: a neurophysiological approach. Pathophysiology . 2010;17:19–28.
Chapter 19 Occipital Nerve Block

Indications and Clinical Considerations
Occipital nerve block is useful in the diagnosis and treatment of occipital neuralgia. Occipital neuralgia is usually the result of blunt trauma to the greater and lesser occipital nerves. Repetitive microtrauma from working with the neck hyperextended (e.g., painting ceilings or working for prolonged periods with computer monitors whose focal point is too high, causing extension of the cervical spine) also may cause occipital neuralgia. The pain of occipital neuralgia is characterized as persistent pain at the base of the skull with occasional sudden, shocklike paresthesias in the distribution of the greater and lesser occipital nerves. Tension-type headache, which is much more common than occipital neuralgia, occasionally mimics the pain of occipital neuralgia, as can intracranial neoplasms ( Figure 19-1 ).

Figure 19-1 Preoperative computed tomography three-dimensional reconstruction reveals a multiloculated cystic mass in the lower portion of the occipital bone, characterized by an increased volume of the dipole with eggshell-like outer and inner plates.
(From Han X, Dong Y, Sun K, Lu Y: A huge occipital osteoblastoma accompanied with aneurysmal bone cyst in the posterior cranial fossa, Clin Neurol Neurosurg 110:282-285, 2008.)

Clinically Relevant Anatomy
The greater occipital nerve arises from fibers of the dorsal primary ramus of the second cervical nerve and, to a lesser extent, fibers from the third cervical nerve. The greater occipital nerve pierces the fascia just below the superior nuchal ridge along with the occipital artery. It supplies the medial portion of the posterior scalp as far anterior as the vertex ( Figure 19-2 ).

Figure 19-2 When the occipital nerve is injected, care must be taken to avoid entering the foramen magnum.
The lesser occipital nerve arises from the ventral primary rami of the second and third cervical nerves. The lesser occipital nerve passes superiorly along the posterior border of the sternocleidomastoid muscle, dividing into cutaneous branches that innervate the lateral portion of the posterior scalp and the cranial surface of the pinna of the ear (see Figure 19-2 ).

Technique
The patient is placed in a sitting position with the cervical spine flexed and the forehead on a padded bedside table. A total of 8 mL of local anesthetic is drawn up in a 19-mL sterile syringe. When occipital neuralgia or other painful conditions involving the greater and lesser occipital nerve are treated, a total of 80 mg of methylprednisolone is added to the local anesthetic with the first block, and 40 mg of methylprednisolone is added with subsequent blocks.
The occipital artery is then palpated at the level of the superior nuchal ridge. After preparation of the skin with antiseptic solution, a 22-gauge, 1½-inch needle is inserted just medial to the artery and is advanced perpendicularly until the needle approaches the periosteum of the underlying occipital bone. A paresthesia may be elicited; the patient should be warned of this. The needle is then redirected superiorly, and after gentle aspiration 5 mL of solution is injected in a fanlike distribution with care being taken to avoid the foramen magnum, which is located medially (see Figure 19-2 ).
The lesser occipital nerve and a number of superficial branches of the greater occipital nerve are then blocked by directing the needle laterally and slightly inferiorly. After gentle aspiration, an additional 3 to 4 mL of solution is injected. Recently, the use of ultrasound guidance for needle placement has been used in selected patients undergoing occipital nerve block ( Figure 19-3 ). In the rare patient with intractable occipital neuralgia, stimulation of the affected occipital nerves via implanted electrode may be of value.

Figure 19-3 Ultrasound short-axis view at the first cervical nerve (C1) level showing the greater occipital nerve (arrowhead). IOM, Inferior oblique muscle; SSC, semispinalis capitis; Spl, splenius muscle; Trap, trapezius muscle; SC, subcutaneous tissue; Med., medial; Lat., lateral. Note: At this level, the greater occipital nerve is more than 1 cm deep to the subcutaneous tissue (separated by the semispinalis capitis muscle).
(From Narouze S: Ultrasound in chronic pain management, Tech Reg Anesth Pain Manag 13:198-202, 2009.)

Side Effects and Complications
The scalp is highly vascular and this, coupled with the fact that both nerves are in proximity to arteries, means that the pain specialist should carefully calculate the total milligram dose of local anesthetic that may be safely given, especially if bilateral nerve blocks are being performed. This vascularity and proximity to the arterial supply gives rise to an increased incidence of postblock ecchymosis and hematoma formation. These complications can be decreased if manual pressure is applied to the area of the block immediately after injection. In spite of the vascularity of this anatomic region, this technique can be safely performed in the presence of anticoagulation with a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. Application of cold packs for 20-minute periods after the block also decreases the amount of postprocedure pain and bleeding the patient may experience.
As mentioned previously, care must be taken to avoid inadvertent needle placement into the foramen magnum because subarachnoid administration of local anesthetic in this region will result in immediate total spinal anesthesia.

Clinical Pearls
The most common reason that greater and lesser occipital nerve block fails to relieve headache pain is that the headache syndrome being treated has been misdiagnosed as occipital neuralgia. Occipital neuralgia is an infrequent cause of headaches and rarely occurs in the absence of trauma to the greater and lesser occipital nerves. More often, the patient with headaches that involve the occipital region is in fact experiencing tension-type headaches. Tension-type headaches do not respond to occipital nerve blocks but are very amenable to treatment with antidepressant compounds (such as amitriptyline) in conjunction with cervical steroid epidural nerve blocks. Therefore the clinician should reconsider the diagnosis of occipital neuralgia in patients whose symptoms are consistent with occipital neuralgia but fail to respond to greater and lesser occipital nerve blocks.
Any patient with headaches severe enough to require neural blockade as part of the treatment plan should undergo magnetic resonance imaging of the head to rule out unsuspected intracranial pathology. Furthermore, cervical spine radiographs should be considered to rule out congenital abnormalities such as Arnold-Chiari malformation, which may be the hidden cause of the patient’s occipital headaches.


Suggested Readings

Fernández-de-Las-Peñas C., Alonso-Blanco C., Cuadrado M.L., Pareja J.A. Myofascial trigger points in the suboccipital muscles in episodic tension-type headache. Man Ther . 2006;11:225–230.
Levin M. Nerve blocks in the treatment of headache. Neurotherapeutics . 2010;7:197–203.
Paemeleire K., Bartsch T. Occipital nerve stimulation for headache disorders. Neurotherapeutics . 2010;7:213–219.
Waldman S.D. Greater and lesser occipital nerve block. In: In Pain review . Philadelphia: Saunders; 2009:393–394.
Waldman S.D. Occipital neuralgia. In In Atlas of common pain syndromes , ed 2, Philadelphia: Saunders; 2008:23–25.
Waldman S.D. The greater and lesser occipital nerves. In: In Pain review . Philadelphia: Saunders; 2009:41–42.
Chapter 20 Injection Technique for Splenius Cervicis Syndrome

Indications and Clinical Considerations
The splenius cervicis is susceptible to the development of myofascial pain syndrome. Flexion-extension and lateral motion stretch injuries to the neck and upper back or repeated microtrauma secondary to jobs that require working overhead or looking to one side for long periods such as painting ceilings or to activities such as reading in bed or watching television while reclining on a couch may result in the development of myofascial pain in the splenius cervicis muscle.
Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points generally are localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other anatomic areas. This referred pain often is misdiagnosed or attributed to other organ systems, thereby leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the splenius cervicis often have referred pain into the occipital and temporal regions as well as circumferential pain that may mimic tension-type headache.
The trigger point is the pathognomonic lesion of myofascial pain and is thought to be the result of microtrauma to the affected muscles. This pathologic lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain but also referred pain. In addition to local and referred pain, there often is an involuntary withdrawal of the stimulated muscle, called a “jump sign.” This jump sign also is characteristic of myofascial pain syndrome.
Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all of these theories is the belief that trigger points are the result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as a result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit.
In addition to muscle trauma, a variety of other factors seem to predispose the patient to develop myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity may develop myofascial pain syndrome. The poor posture of someone sitting at a computer keyboard or watching television has also been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All of these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The splenius cervicis muscle seems to be particularly susceptible to stress-induced myofascial pain syndrome.
Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

Clinically Relevant Anatomy
The muscles of the neck work together as a functional unit to stabilize and allow coordinated movement of the head and associated sense organs. Trauma to an individual muscle can result in dysfunction of the entire functional unit.
The splenius cervicis muscle begins as a narrow tendinous band that attaches to the spinous processes of the third through sixth thoracic vertebra ( Figure 20-1 ). The muscle extends upward and inserts via the tendinous fasciculi into the posterior tubercles of the transverse processes of the second and third cervical vertebrae. The splenius cervicis muscles are innervated by the respective lateral branches of the posterior divisions of the middle and lower cervical nerves. The muscle on each side of the neck can act independently to assist in lateral rotation and bending of the neck. The splenius cervicis muscles act together to help extend the cervical spine and pull the head posteriorly. A secondary function of these muscles is to help support and strengthen the deeper muscles of the posterior neck.

Figure 20-1 The splenius cervicis muscle begins as a fibrous tendon that attaches to the spinous processes of the third through sixth thoracic vertebra.
The points of insertion of the splenius cervicis on the cervical vertebra are particularly susceptible to trauma and the subsequent development of myofascial trigger points (see Figure 20-1 ). Injection of these trigger points serves as both a diagnostic and a therapeutic maneuver.

Technique
Careful preparation of the patient before trigger point injection helps to optimize results. Trigger point injections are directed at the primary trigger point rather than in the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and thus, it is hoped, provide long-lasting relief. It is important for the patient to understand that for most patients with myofascial pain syndrome, more than one treatment modality is required for optimal pain relief. The use of the recumbent or lateral position when identifying and marking trigger points, as well as when performing the actual trigger point injection, helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection.
After the goals of trigger point injection have been explained to the patient and proper preparation of the patient has been carried out, the trigger point is reidentified by palpation with the sterilely gloved finger. A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25- or 27-gauge needle of a length adequate to reach the trigger point. Except for the muscles of posture in the low back, a 1½-inch needle will be adequate. A volume of 0.5 to 1.0 mL of solution is then injected into each trigger point. A series of two to five treatment sessions may be required to completely abolish the trigger point; the patient should be informed of this.

Side Effects and Complications
The proximity to the spinal cord and exiting cervical nerve roots makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing interventional pain management techniques. Given the proximity of the brain and brainstem, ataxia caused by vascular uptake of local anesthetic after trigger point injection is not an uncommon occurrence. Many patients also complain of a transient increase in pain after injection of trigger points in the splenius cervicis.

Clinical Pearls
Trigger point injections are extremely safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space.
The antidepressant compounds represent the primary pharmacologic treatment for myofascial pain syndrome. The tricyclic antidepressants are thought to be more effective than the selective serotonin reuptake inhibitors in the treatment of this painful condition. The precise mechanism of action of the antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome. Drugs such as amitriptyline and nortriptyline represent good first choices and should be given as a single bedtime dose, starting with 10 to 25 mg and titrating upward as side effects allow. Pregabalin may also be of value in the pharmacologic management of myofascial pain syndromes.


Suggested Readings

Baldry P. Acupuncture treatment of fibromyalgia and myofascial pain. In: Chaitow L., ed. Fibromyalgia syndrome . ed 3. Oxford: Churchill Livingstone; 2010:145–159.
Ge H.Y., Nie H., Madeleine P., et al. Contribution of the local and referred pain from active myofascial trigger points in fibromyalgia syndrome. Pain . 2009;147:233–240.
Ge H.Y., Wang Y., Danneskiold-Samsøe B., et al. The predetermined sites of examination for tender points in fibromyalgia syndrome are frequently associated with myofascial trigger points. J Pain . 2010;11:644–651.
LeBlanc K.E., LeBlanc L.L. Musculoskeletal disorders. Prim Care . 2010;37:389–406.
Lucas K.R., Rich P.A., Polus B.I. Muscle activation patterns in the scapular positioning muscles during loaded scapular plane elevation: the effects of latent myofascial trigger points. Clin Biomech (Bristol, Avon) . 2010;25:765–770.
Partanen J.V., Ojala T.A., Arokoski J.P. Myofascial syndrome and pain: a neurophysiological approach. Pathophysiology . 2010;17:19–28.
Section 2
Shoulder
Chapter 21 Intraarticular Injection of the Shoulder Joint

Indications and Clinical Considerations
The shoulder joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage. Osteoarthritis of the joint is the most common form of arthritis that results in shoulder joint pain. However, rheumatoid arthritis, posttraumatic arthritis, and rotator cuff tear arthropathy are also common causes of shoulder pain secondary to arthritis. Less common causes of arthritis-induced shoulder pain include the collagen vascular diseases, infection, villonodular synovitis, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics rather than with injection therapy. The collagen vascular diseases generally manifest as a polyarthropathy rather than a monoarthropathy limited to the shoulder joint, although shoulder pain secondary to collagen vascular disease responds exceedingly well to the intraarticular injection technique described later.
In most patients with shoulder pain secondary to osteoarthritis, rotator cuff arthropathy, and posttraumatic arthritis pain, the pain is localized around the shoulder and upper arm. Activity makes the pain worse, and rest and heat provide some relief. The pain is constant and characterized as aching. The pain may interfere with sleep. Some patients report a grating or popping sensation with use of the joint, and crepitus may be present on physical examination.
In addition to the just-described pain, patients with arthritis of the shoulder joint often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks, such as hair combing, fastening a bra, or reaching overhead, difficult. With continued disuse, muscle wasting may occur, and a frozen shoulder may develop.
Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the shoulder is indicated if a rotator cuff tear is suspected.

Clinically Relevant Anatomy
The rounded head of the humerus articulates with the pear-shaped glenoid fossa of the scapula ( Figure 21-1 ). The articular surface is covered with hyaline cartilage, which is susceptible to arthritis. The rim of the glenoid fossa is composed of a fibrocartilaginous layer called the glenoid labrum, which is susceptible to trauma should the humerus be subluxed or dislocated. The joint is surrounded by a relatively lax capsule that allows the wide range of motion of the shoulder joint at the expense of decreased joint stability. The joint capsule is lined with a synovial membrane that attaches to the articular cartilage. This membrane gives rise to synovial tendon sheaths and bursae that are subject to inflammation. The shoulder joint is innervated by the axillary and suprascapular nerves.

Figure 21-1 Normal anatomy of the shoulder. A, Acromion; B, intertubercular groove (bicipital groove); C, coracoid; G, glenoid; Na, anatomic neck; N s , surgical neck; T g , greater tubercle; T l , lesser tubercle.
(From Houston JD, Davis M: Fundamentals of fluoroscopy, Philadelphia, 2001, Saunders.)
The major ligaments of the shoulder joint are the glenohumeral ligaments in front of the capsule, the transverse humeral ligament between the humeral tuberosities, and the coracohumeral ligament, which stretches from the coracoid process to the greater tuberosity of the humerus ( Figure 21-2 ). Along with the accessory ligaments of the shoulder, these major ligaments provide strength to the shoulder joint. The strength of the shoulder joint also is dependent on short muscles that surround the joint: the subscapularis, the supraspinatus, the infraspinatus, and the teres minor. These muscles and their attaching tendons are susceptible to trauma and to wear and tear from overuse and misuse.

Figure 21-2 The rounded head of the humerus articulates with the pear-shaped glenoid fossa of the scapula.

Technique
The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the shoulder, subacromial region, and joint space is carried out. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle with strict aseptic technique. With strict aseptic technique the midpoint of the acromion is identified, and at a point approximately 1 inch below the midpoint the shoulder joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues and through the joint capsule into the joint (see Figure 21-2 ). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected superiorly and slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be little resistance to injection. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. In patients in whom the anatomic landmarks are difficult to identify, fluoroscopic or ultrasound guidance for needle placement may be beneficial ( Figures 21-3 and 21-4 ).

Figure 21-3 Proper ultrasound transducer placement for intraarticular injection of the glenohumeral joint.

Figure 21-4 Intraarticular injection of the shoulder (arrowheads). Note the bare humeral head with cortical irregularity indicative of osteoarthritis (arrow).

Side Effects and Complications
The major complication of intraarticular injection of the shoulder is infection. This complication should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients report a transient increase in pain after intraarticular injection of the shoulder joint; the patient should be warned of this.

Clinical Pearls
This injection technique is extremely effective in the treatment of pain secondary to the previously mentioned causes of arthritis of the shoulder joint. Coexistent bursitis and tendinitis also may contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it will exacerbate the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Suggested Reading

Andrews J.R. Diagnosis and treatment of chronic painful shoulder: Review of nonsurgical interventions. Arthroscopy . 2005;21:333–347.
Cheng P.H., Modir J.G., Kim H.J., Narouze S. Ultrasound-guided shoulder joint injections. Tech Reg Anesth Pain Manag . 2009;13:184–190.
Dalton S.E. Clinical examination of the painful shoulder. Baillieres Clin Rheumatol . 1989;3:453–474.
Davies A.M. Imaging the painful shoulder. Curr Orthop . 1992;6:32–38.
Monach P.A. Shoulder pain. In: Mushlin S.B., Greene H.L. Decision making in medicine: an algorithmic approach . ed 3. Philadelphia: Mosby; 2010:522–523.
Reutter T.R.C. Shoulder pain. In: Ramamurthy S., Rogers J.N., Alanmanou E. Decision making in pain management . ed 2. Philadelphia: Mosby; 2006:160–162.
Chapter 22 Acromioclavicular Joint Injection

Indications and Clinical Considerations
The acromioclavicular joint is vulnerable to injury from both acute trauma and repetitive microtrauma. Acute injuries frequently take the form of falls directly onto the shoulder when playing sports or falling from a bicycle. Repeated strain from throwing injuries or working with the arm raised across the body also may result in trauma to the joint. After trauma the joint may become acutely inflamed, and if the condition becomes chronic, arthritis of the acromioclavicular joint may develop.
The patient with acromioclavicular joint pain frequently reports increased pain when reaching across the chest. Often the patient is unable to sleep on the affected shoulder and may report a grinding sensation in the joint, especially on first awakening. Physical examination may reveal enlargement or swelling of the joint with tenderness to palpation. Downward traction or passive adduction of the affected shoulder may cause increased pain. The chin adduction test will also help confirm the diagnosis. This test is performed by having the patient abduct the affected arm to 90 degrees and then adduct the arm across the chest just under the chin with the objective of grasping the contralateral shoulder ( Figure 22-1 ). Patients with acromioclavicular joint dysfunction will experience severe pain and often will be unable to repeat the maneuver. Furthermore, if there is disruption of the ligaments of the acromioclavicular joint, these maneuvers may reveal joint instability. Plain radiographs of the joint may reveal narrowing or sclerosis of the joint consistent with osteoarthritis or widening of the joint consistent with ligamentous injury ( Figure 22-2 ). Magnetic resonance imaging (MRI) is indicated if disruption of the ligaments is suspected or if a clear cause of the patient’s pain has not been found ( Figure 22-3 ). The injection technique described later serves as both a diagnostic and a therapeutic maneuver.

Figure 22-1 The chin adduction test for acromioclavicular joint dysfunction.
(From Waldman SD: Physical Diagnosis of Pain , ed 2, Philadelphia, 2010, Saunders.)

Figure 22-2 Widening of the acromioclavicular joint after disruption of the acromioclavicular ligament (arrow).
(From Resnick D, Kang HS: Internal derangements of joints: emphasis on MR imaging, Philadelphia, 1997, Saunders.)

Figure 22-3 Osteoarthritis of the acromioclavicular joint: synovial cyst formation. An oblique coronal fat-suppressed fast spin-echo (TR/TE, 2750/100) magnetic resonance image shows deformity of the distal portion of the clavicle related to osteoarthritis and a synovial cyst (arrow) containing fluid derived from the acromioclavicular joint.
(From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)

Clinically Relevant Anatomy
The acromioclavicular joint is formed by the distal end of the clavicle and the anterior and medial aspects of the acromion ( Figure 22-4 ). The strength of the joint arises in large part from the dense coracoclavicular ligament, which attaches the bottom of the distal end of the clavicle to the coracoid process. A small indentation can be felt where the clavicle abuts the acromion. The joint is completely surrounded by an articular capsule. The superior portion of the joint is covered by the superior acromioclavicular ligament, which attaches the distal clavicle to the upper surface of the acromion. The inferior portion of the joint is covered by the inferior acromioclavicular ligament, which attaches the inferior portion of the distal clavicle to the acromion. Both of these ligaments further add to the joint’s stability. The acromioclavicular joint may or may not contain an articular disk. The volume of the acromioclavicular joint space is small, and care must be taken not to disrupt the joint by forcefully injecting large volumes of local anesthetic and corticosteroid into the intraarticular space when performing this injection technique.

Figure 22-4 The acromioclavicular joint is located approximately 1 inch medial to the acromion.

Technique
The goals of this injection technique are explained to the patient. The patient is placed in the supine position, and proper preparation with antiseptic solution of the skin overlying the superior shoulder and distal clavicle is carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique the top of the acromion is identified, and at a point approximately 1 inch medially the acromioclavicular joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues medially at a 20-degree angle through the joint capsule into the joint (see Figure 22-4 ). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and redirected slightly more medially. After the joint space has been entered, the contents of the syringe are gently injected. There should be some resistance to injection, because the joint space is small and the joint capsule is dense. If significant resistance is encountered, the needle is probably in a ligament and should be advanced or withdrawn slightly into the joint space until the injection proceeds with only limited resistance. If no resistance is encountered on injection, the joint space is probably not intact and MRI of the joint is recommended. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site. In patients in whom the anatomic landmarks are difficult to identify, fluoroscopic or ultrasound guidance for needle placement may be beneficial ( Figures 22-5 and 22-6 ).

Figure 22-5 Proper transducer positioning for ultrasound-guided acromioclavicular joint injection.

Figure 22-6 Ultrasound-guided intraarticular needle placement in the acromioclavicular joint. The bright spot indicates the tip of the needle (circle).
(From Sabeti-Aschraf M, Ochsner A, Schueller-Weidekamm C, et al: The infiltration of the AC joint performed by one specialist: ultrasound versus palpation a prospective randomized pilot study, Eur J Radiol 75: e37-e40, 2010.)

Side Effects and Complications
The major complication of intraarticular injection of the acromioclavicular joint is infection. This complication should be exceedingly rare if strict aseptic technique is followed. As mentioned previously, forceful injection into the joint may disrupt the joint capsule and should be avoided. Approximately 25% of patients report a transient increase in pain after intraarticular injection of this joint; the patient should be warned of this.

Clinical Pearls
This injection technique is extremely effective in the treatment of pain secondary to the just-described causes of arthritis of the acromioclavicular joint. Coexistent bursitis and tendinitis also may contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot corticosteroid. This technique is safe if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Suggested Readings

Andrews J.R. Diagnosis and treatment of chronic painful shoulder: Review of nonsurgical interventions. Arthroscopy . 2005;21:333–347.
Cheng P.H., Modir J.G., Kim H.J., Narouze S. Ultrasound-guided shoulder joint injections. Tech Reg Anesth Pain Manag . 2009;13:184–190.
Dalton S.E. Clinical examination of the painful shoulder. Baillieres Clin Rheumatol . 1989;3:453–474.
Davies A.M. Imaging the painful shoulder. Curr Orthop . 1992;6:32–38.
Monach P.A. Shoulder pain. In: Mushlin S.B., Greene H.L. Decision making in medicine: an algorithmic approach . ed 3. Philadelphia: Mosby; 2010:522–523.
Reutter T.R.C. Shoulder pain. In: Ramamurthy S., Rogers J.N., Alanmanou E. Decision making in pain management . ed 2. Philadelphia: Mosby; 2006:160–162.
Chapter 23 Supraspinatus Tendon Injection

Indications and Clinical Considerations
The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions that are often repetitive. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult ( Figure 23-1 ). Tendinitis of the musculotendinous unit of the shoulder frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability.

Figure 23-1 Intervertebral osteochondrosis: Pathologic abnormalities. Four coronal sections reveal the varied pathologic changes of intervertebral osteochondrosis. In the initial stages of the disease (A), cracks or crevices in the nucleus pulposus become evident (arrows). With progression (B), the fissures enlarge and involve portions of the nucleus pulposus and anulus fibrosus (arrows). Intervertebral disk space loss and condensation of bone in the vertebral bodies (arrowheads) become evident. With the onset of abnormalities of the anulus fibrosus, triangular osteophytes may be seen (open arrows).
(From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders.)
The supraspinatus tendon of the rotator cuff is particularly prone to the development of tendinitis. The onset of supraspinatus tendinitis is usually acute, occurring after overuse or misuse of the shoulder joint. Inciting factors may include carrying heavy loads in front and away from the body or the vigorous use of exercise equipment. The pain is constant and severe, with sleep disturbance often reported. The patient may attempt to splint the inflamed tendon by elevating the scapula to remove tension from the ligament, giving the patient a “shrugging” appearance. Patients with supraspinatus tendinitis exhibit a positive Dawbarn sign—pain on palpation over the greater tuberosity of the humerus when the arm is hanging down that disappears when the arm is fully abducted.
In addition to the just-described pain, patients with supraspinatus tendinitis often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks, such as hair combing, fastening a bra, or reaching overhead, difficult. With continued disuse, muscle wasting may occur and a frozen shoulder may develop.
Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the shoulder is indicated if a rotator cuff tear is suspected. Ultrasound evaluation of the affected area may also help delineate the presence of calcific tendinitis or other shoulder disease ( Figure 23-2 ). The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

Figure 23-2 Examples of “hard calcification” that typify the formative phase of calcific tendinosis. A, The anteroposterior radiograph of patient A shows a large, sharply circumscribed calcification within the infraspinatus tendon (solid arrow). B, In patient B, the supraspinatus tendon is imaged longitudinally. A large intratendinous calcification (open arrow) produces significant posterior acoustic shadowing artifact.
(From Louis LJ: Musculoskeletal ultrasound intervention: principles and advances, Ultrasound Clin 4:217–236, 2009.)

Clinically Relevant Anatomy
The supraspinatus muscle is the most important muscle of the rotator cuff. It provides joint stability and, with the deltoid muscle, adducts the arm at the shoulder by fixing the head of the humerus firmly against the glenoid fossa. The supraspinatus muscle is innervated by the suprascapular nerve, has its origin from the supraspinous fossa of the scapula, and inserts into the upper facet of the greater tuberosity of the humerus ( Figure 23-3 ). The muscle passes across the superior aspect of the shoulder joint, with the inferior portion of the tendon intimately involved with the joint capsule. The supraspinatus muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse, as mentioned previously.

Figure 23-3 The supraspinatus tendon of the rotator cuff is particularly prone to the development of tendinitis.

Technique
The goals of this injection technique are explained to the patient. The patient is placed in the supine position with the forearm medially rotated behind the back. If the patient cannot tolerate this position, the injection alternatively may be done with the patient in the sitting position, albeit with greater risk of vasovagal attack. This positioning of the upper extremity places the lateral epicondyle of the elbow in an anterior position and makes its identification easier. After the lateral epicondyle of the elbow has been identified, the humerus is traced superiorly to the anterior edge of the acromion. A slight indentation just below the anterior edge of the acromion marks the point of insertion of the supraspinatus tendon into the upper facet of the greater tuberosity of the humerus. The point is marked with a sterile marker.
Proper preparation with antiseptic solution of the skin overlying the shoulder, subacromial region, and joint space is then carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle using strict aseptic technique. With strict aseptic technique, the previously marked point is palpated and the indentation indicating the insertion of the supraspinatus tendon is reidentified with the gloved finger. The needle is then carefully advanced perpendicularly at this point through the skin and subcutaneous tissues, through the joint capsule, until it impinges on bone (see Figure 23-2 ). The needle is then withdrawn 1 to 2 mm out of the periosteum of the humerus, and the contents of the syringe are gently injected. There should be slight resistance to injection. If no resistance is encountered, either the needle tip is in the joint space itself or the supraspinatus tendon is ruptured. If there is significant resistance to injection, the needle tip is probably in the substance of a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site.

Side Effects and Complications
The major complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is followed. Trauma to the supraspinatus tendon from the injection itself remains an ever-present possibility. Tendons that are highly inflamed or previously damaged are subject to rupture if they are directly injected. This risk of this complication can be greatly decreased if the clinician uses gentle technique and stops injecting immediately if significant resistance to injection is encountered. Approximately 25% of patients report a transient increase in pain after this injection technique; the patient should be warned of this.

Clinical Pearls
This injection technique is extremely effective in the treatment of pain secondary to the just-described causes of shoulder pain. Coexistent bursitis and arthritis also may contribute to shoulder pain and may require additional treatment with a more localized injection of local anesthetic and depot corticosteroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection; universal precautions should be used to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient has undergone this injection technique for shoulder pain. Vigorous exercise should be avoided because it exacerbates the patient’s symptoms. Simple analgesics and nonsteroidal antiinflammatory agents may be used concurrently with this injection technique.

Suggested Readings

Andrews J.R. Diagnosis and treatment of chronic painful shoulder: Review of nonsurgical interventions. Arthroscopy . 2005;21:333–347.
Cheng P.H., Modir J.G., Kim H.J., Narouze S. Ultrasound-guided shoulder joint injections. Tech Reg Anesth Pain Manag . 2009;13:184–190.
Dalton S.E. Clinical examination of the painful shoulder. Baillieres Clin Rheumatol . 1989;3:453–474.
Davies A.M. Imaging the painful shoulder. Curr Orthop . 1992;6:32–38.
Monach P.A. Shoulder pain. In: Mushlin S.B., Greene H.L. Decision making in medicine: an algorithmic approach . ed 3. Philadelphia: Mosby; 2010:522–523.
Reutter T.R.C. Shoulder pain. In: Ramamurthy S., Rogers J.N., Alanmanou E. Decision making in pain management . ed 2. Philadelphia: Mosby; 2006:160–162.
Yoo J.C., Koh K.H., Park W.H., et al. The outcome of ultrasound-guided needle decompression and steroid injection in calcific tendinitis. J Shoulder Elbow Surg . 2010;19:596–600.
Chapter 24 Infraspinatus Tendon Injection

Indications and Clinical Considerations
The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of motions, which are often repetitive. Second, the space in which the musculotendinous unit functions is restricted by the coracoacromial arch, making impingement a likely possibility with extreme movements of the joint. Third, the blood supply to the musculotendinous unit is poor, making healing of microtrauma more difficult. All of these factors can contribute to tendinitis of one or more of the tendons of the shoulder joint. Calcium deposition around the tendon may occur if the inflammation continues, making subsequent treatment more difficult. Tendinitis of the musculotendinous unit of the shoulder frequently coexists with bursitis of the associated bursae of the shoulder joint, creating additional pain and functional disability.
The infraspinatus tendon of the rotator cuff is particularly prone to the development of tendinitis ( Figure 24-1 ). The onset of infraspinatus tendinitis is usually acute, occurring after overuse or misuse of the shoulder joint. Inciting factors may include activities that require repeated abduction and lateral rotation of the humerus, such as installing brake pads during assembly line work. The vigorous use of exercise equipment also has been implicated. The pain of infraspinatus tendinitis is constant, severe, and localized in the deltoid area. Significant sleep disturbance is often reported. The patient may attempt to splint the inflamed infraspinatus tendon by rotating the scapula anteriorly to remove tension from the tendon. Patients with infraspinatus tendinitis exhibit pain with lateral rotation of the humerus and on active abduction ( Figure 24-2 ).

Figure 24-1 Magnetic resonance image showing severe tendinosis of the infraspinatus tendon.
(From Adler RS, Finzel KC: The complementary roles of MR imaging and ultrasound of tendons, Radiol Clin North Am 34:771–807, 2005, with permission.)

Figure 24-2 A and B, The mid-arc abduction test for infraspinatus tendinitis will reveal the onset of severe pain in the middle range of the arc with the pain improving as the patient reaches the top of the arc of abduction.
(From Waldman SD: Physical diagnosis of pain, Philadelphia, 2005, Saunders.)
In addition to the just-described pain, patients with infraspinatus tendinitis often experience a gradual decrease in functional ability with decreasing shoulder range of motion, making simple everyday tasks, such as hair combing, fastening a bra, or reaching overhead, difficult. With continued disuse, muscle wasting may occur, and a frozen shoulder may develop.
Plain radiographs are indicated for all patients with shoulder pain. On the basis of the patient’s clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and/or ultrasound imaging of the shoulder is indicated if a rotator cuff tear is suspected. The injection technique presented later serves as both a diagnostic and a therapeutic maneuver.

Clinically Relevant Anatomy
The infraspinatus muscle is part of the rotator cuff. It provides shoulder joint stability and, along with the teres minor muscle, externally rotates the arm at the shoulder. The infraspinatus muscle is innervated by the suprascapular nerve. The infraspinatus muscle has its origin in the infraspinous fossa of the scapula and inserts into the middle facet of the greater tuberosity of the humerus. It is at this insertion that infraspinatus tendinitis most commonly occurs ( Figure 24-3 ). The infraspinatus muscle and tendons are susceptible to trauma and to wear and tear from overuse and misuse, as mentioned previously.

Figure 24-3 Patients with infraspinatus tendinitis will often experience excellent pain relief with injection of the tendon with steroid and local anesthetic.

Technique
The goals of this injection technique are explained to the patient. The patient is placed in the sitting position with the arm supported on a bedside table and flexed to 90 degrees at the elbow. The arm is then externally rotated, which brings the insertion of the infraspinatus tendon out from under the deltoid muscle. The infraspinatus muscle can be felt to contract with this maneuver. The posterior angle of the acromion is then identified, as is the lateral epicondyle at the elbow. In this position the insertion of the infraspinatus tendon is in a direct line with the lateral epicondyle of the elbow. The insertion should be approximately 45 degrees inferior to the posterior angle of the acromion. The point is marked with a sterile marker.
Proper preparation with antiseptic solution of the skin overlying the posterior shoulder, acromial region, and joint space is then carried out. A sterile syringe containing 1.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1½-inch, 25-gauge needle with strict aseptic technique. With strict aseptic technique, the previously marked point is palpated and the insertion of the infraspinatus tendon is reidentified with the gloved finger.

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